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Professor Joerg Mattes

Chair - Paediatrics & Child Health

School of Medicine and Public Health (Immunology and Microbiology)

Career Summary

Biography

Joerg Mattes' research has focused on the pathogenesis of asthma, allergies and respiratory infections. The major sequence of recent projects undertaken in this area has involved clinical trials (e.g. the effect of asthma management/smoke cessation interventions during pregnancy on respiratory outcomes/lung function in the offspring; high-flow oxygen for the management of moderate severe bronchiolitis), clinical studies (e.g. biomarkers of peanut allergy and eosinophilic oesophagitis), experimental studies in asthma, rhinovirus infection and eosinophilic oesophagitis (e.g. role of micro(mi)RNAs; Midline-1). Some of his most significant research outcomes are published in The Lancet, Nature Medicine, Journal of Experimental Medicine, and Proceedings of the National Academy of Sciences. The works received prizes and awards.

Research Expertise
microRNAs; rhinovirus infection; asthma; infant lung function; high flow oxygen; eosinophilic oesophagitis; cardiopulmonary exercise testing; TRAIL; midline-1


Qualifications

  • Habilitation (European Equiv to Doctor of Sc), University of Freiburg - Germany
  • Doctor of Medicine, University of Hamburg - Germany

Keywords

  • Asthma and wheezing
  • Immunology
  • Infant lung function
  • Paediatrics
  • Respiratory Diseases
  • Rhinovirus
  • Virology

Languages

  • German (Fluent)

Fields of Research

Code Description Percentage
060499 Genetics not elsewhere classified 10
110399 Clinical Sciences not elsewhere classified 25
110799 Immunology not elsewhere classified 65

Professional Experience

UON Appointment

Title Organisation / Department
Chair - Paediatrics & Child Health University of Newcastle
School of Medicine and Public Health
Australia
Chair - Paediatrics & Child Health Priority Research Centre (PRC) for Healthy Lungs | The University of Newcastle
School of Medicine and Public Health
Australia
Chair - Paediatrics & Child Health University of Newcastle
School of Medicine and Public Health
Australia

Academic appointment

Dates Title Organisation / Department
1/12/2007 - 1/12/2011 Health Professional Research Fellowship (Part-time)

NHMRC - Early Career Fellowships (Formerly Postdoctoral Training Fellowships)

University of Newcastle
School of Medicine and Public Health
Australia
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Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Chapter (2 outputs)

Year Citation Altmetrics Link
2015 Maltby S, Plank M, Ptaschinski C, Mattes J, Foster PS, 'MicroRNA function in mast cell biology: Protocols to characterize and modulate MicroRNA expression', Mast Cells: Methods and Protocols, Springer, New York 287-304 (2015) [B1]
DOI 10.1007/978-1-4939-1568-2_18
Citations Scopus - 7
Co-authors Steven Maltby, Paul Foster
2013 Lee JJ, Ptaschinski C, Plank M, Mattes J, Foster PS, Balla KM, et al., 'Emerging Concepts', Eosinophils in Health and Disease, Academic Press, London 607-641 (2013) [B1]
DOI 10.1016/B978-0-12-394385-9.00016-X
Co-authors Paul Foster

Journal article (116 outputs)

Year Citation Altmetrics Link
2020 Mattes J, Collison A, 'Fetal Eosinophils Get on the Nerves of Airways Early Origins of Bronchoconstriction', AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 62 407-408 (2020)
DOI 10.1165/rcmb.2019-0438ED
Co-authors Adam Collison
2020 Harvey SM, Murphy VE, Gibson PG, Collison A, Robinson P, Sly PD, et al., 'Maternal asthma, breastfeeding, and respiratory outcomes in the first year of life', Pediatric Pulmonology, 55 1690-1696 (2020) [C1]

© 2020 Wiley Periodicals, Inc. Maternal asthma increases the risk of infant wheeze. Breastfeeding may offer protection but there is limited evidence in this high-risk group. We ex... [more]

© 2020 Wiley Periodicals, Inc. Maternal asthma increases the risk of infant wheeze. Breastfeeding may offer protection but there is limited evidence in this high-risk group. We examined associations between breastfeeding and respiratory outcomes, in infants born to women with asthma. This study was a secondary analysis of two prospective cohorts of pregnant women with asthma, and their infants, conducted between 2007 and 2018. At 6 ± 1 (T1) and 12 ± 1 (T2) months post-partum, mothers reported breastfeeding patterns and infant wheeze (primary outcome), bronchiolitis, and related medication use and healthcare utilization, via a validated questionnaire; a subgroup completed face-to-face interviews. ¿2 tests and logistic regression models, adjusting for confounders, were utilized. Data were complete for 605 participants at T1 and 486 (80%) at T2. Of 605 participants: 89% initiated breastfeeding and 38% breastfed for more than 6 months. Breastfeeding for more than 6 months vs ¿never¿ was associated with a reduced adjusted relative risk of infant wheeze at T1 (0.54, 95% confidence interval, 0.30-0.96). Bronchiolitis risk was reduced at T1 and T2 with more tha 6 months of breastfeeding vs ¿never.¿ Breastfeeding duration of 1 to 3 months, 4 to 6 months, and more than 6 months were associated with a reduced risk of infant healthcare utilization (all P <.05, vs ¿never¿), but not medication use (P >.05). Breastfeeding for more than 6 months was associated with a reduced risk of wheeze, bronchiolitis, and wheeze-related healthcare utilization in infants at risk due to maternal asthma. Notably, breastfeeding for shorter durations was associated with a reduced risk of healthcare utilization compared with none. Larger cohorts are needed to further examine the impact of breastfeeding exposure on respiratory health in infants exposed to maternal asthma.

DOI 10.1002/ppul.24756
Co-authors Vanessa Murphy, Peter Gibson, Adam Collison, Megan Jensen
2020 Perkes S, Bonevski B, Mattes J, Hall K, Gould GS, 'Respiratory, birth and health economic measures for use with Indigenous Australian infants in a research trial: a modified Delphi with an Indigenous panel', BMC Pediatrics, 20 (2020) [C1]
DOI 10.1186/s12887-020-02255-x
Co-authors Billie Bonevski, Gillian Gould
2020 Percival E, Bhatia R, Preece K, McEvoy M, Collison A, Mattes J, 'Change in exhaled nitric oxide during peanut challenge is related to severity of reaction', ALLERGY ASTHMA AND CLINICAL IMMUNOLOGY, 16 (2020) [C1]
DOI 10.1186/s13223-020-00464-8
Co-authors Mark Mcevoy, Adam Collison
2020 Whalen OM, Campbell LE, Murphy VE, Lane AE, Gibson PG, Mattes J, et al., 'Observational study of mental health in asthmatic women during the prenatal and postnatal periods', Journal of Asthma, 57 829-841 (2020) [C1]

© 2019, © 2019 Taylor &amp; Francis Group, LLC. Objective: We aimed to examine the prevalence and severity of psychological distress of women with asthma in both the prenatal an... [more]

© 2019, © 2019 Taylor & Francis Group, LLC. Objective: We aimed to examine the prevalence and severity of psychological distress of women with asthma in both the prenatal and postnatal periods, and to determine whether asthmatic women with and without mental health problems differ in self-management, medications knowledge, and asthma symptoms. Methods: We assessed spirometry performance and asthma symptoms in 120 women (mean age 29.8 years) before 23 weeks gestation, as part of the Breathing for Life Trial (Trial ID: ACTRN12613000202763). Prenatal depression data was obtained from medical records. At 6 weeks postpartum, we assessed general health, self-reported asthma control, depression symptoms (with the Edinburgh Postnatal Depression Scale) and adaptive functioning (with the Achenbach System of Empirically Based Assessment scales). Results: Twenty percent of our sample reported having a current mental health diagnosis, 14% reported currently receiving mental health care, while 47% reported having received mental health care in the past (and may/may not have received a diagnosis). The sample scored high on the Aggressive Behavior, Avoidant Personality, and Attention Deficit/Hyperactivity scales. Poorer self-reported postnatal asthma control was strongly correlated with elevated somatic complaints, externalizing problems, antisocial personality problems, and greater withdrawal. Prenatal spirometry or asthma severity and control were largely not associated with measures of psychopathology. Conclusions: These findings indicate that pregnant women with asthma frequently report issues with psychopathology during the prenatal and postnatal periods, and that the subjective perception of asthma control may be more related to psychopathology than objective asthma measures. However, due to sample bias, these findings are likely to be understated.

DOI 10.1080/02770903.2019.1621888
Co-authors Alix Woolard Uon, Alix Woolard, Adam Collison, Alison Lane, Frini Karayanidis, Peter Gibson, Linda E Campbell, Vanessa Murphy
2020 de Gouveia Belinelo P, Nielsen A, Goddard B, Platt L, Da Silva Sena CR, Robinson PD, et al., 'Clinical and lung function outcomes in a cohort of children with severe asthma.', BMC Pulm Med, 20 66 (2020)
DOI 10.1186/s12890-020-1101-6
Co-authors Adam Collison, Peter Gibson, Vanessa Murphy
2020 Murphy VE, Jensen ME, Robijn AL, Wright TK, Mattes J, Collison A, Gibson PG, 'How Maternal BMI Modifies the Impact of Personalized Asthma Management in Pregnancy', Journal of Allergy and Clinical Immunology: In Practice, 8 219-228.e3 (2020) [C1]

© 2019 American Academy of Allergy, Asthma &amp; Immunology Background: Maternal asthma is associated with perinatal complications and respiratory illness in offspring. Obesity ... [more]

© 2019 American Academy of Allergy, Asthma & Immunology Background: Maternal asthma is associated with perinatal complications and respiratory illness in offspring. Obesity increases asthma exacerbation risk in pregnancy and risk of wheeze in offspring. Objectives: In this secondary analysis of a randomized controlled trial, we investigated the influence of maternal body mass index, gestational weight gain (GWG), and fractional exhaled nitric oxide (FENO)-based management on asthma exacerbations in pregnancy and offspring wheeze. Methods: A total of 220 women were randomized to asthma treatment adjustment according to symptoms (control group), or FENO and symptoms (FENO group). Exacerbations were recorded prospectively. Height and weight were measured at baseline, and in late pregnancy. GWG was categorized according to Institute of Medicine guidelines. A validated parent-completed questionnaire assessed infant wheeze-related outcomes. Results: FENO-based management was associated with a significantly lower incidence rate ratio for maternal exacerbations in nonobese mothers (0.52, 95% confidence interval [CI], 0.31-0.88, P = .015, n = 129), and women with GWG within recommendations (0.35, 95% CI, 0.12-0.96, P = .042, n = 43), but not for obese mothers (0.59, 95% CI, 0.32-1.08, P = .089, n = 88), or women with excess GWG (0.58, 95% CI, 0.32-1.04, P = .07, n = 104). Recurrent bronchiolitis occurred in 5.3% (n = 1) of infants born to non-overweight mothers, 16.7% (n = 3) of infants of overweight mothers, and 21.7% (n = 5) of infants of obese mothers in the control group. In the FENO group, 2 infants of obese mothers had recurrent bronchiolitis (7.1%, P = .031). Conclusions: The benefits of FENO-based management are attenuated among obese mothers and those with excess GWG, indicating the importance of weight management in contributing to improved asthma management in pregnancy.

DOI 10.1016/j.jaip.2019.06.033
Citations Scopus - 1Web of Science - 1
Co-authors Adam Collison, Peter Gibson, Vanessa Murphy, Megan Jensen
2020 Silva FMDCE, Oliveira EED, Ambrósio MGE, Ayupe MC, Souza VPD, Gameiro J, et al., 'High-fat diet-induced obesity worsens TH2 immune response and immunopathologic characteristics in murine model of eosinophilic oesophagitis', Clinical and Experimental Allergy, 50 244-255 (2020) [C1]

© 2019 John Wiley &amp; Sons Ltd Background: Eosinophilic oesophagitis (EoE) is an emergent chronic immune-mediated disease of the oesophagus, which affects both children and ad... [more]

© 2019 John Wiley & Sons Ltd Background: Eosinophilic oesophagitis (EoE) is an emergent chronic immune-mediated disease of the oesophagus, which affects both children and adults. It is clinically characterized by dysphagia, food impaction and oesophageal eosinophilia. Epidemiological studies indicate that obesity can worsen allergic symptoms; however, its effect on EoE immunopathological response has not been evaluated yet. This study aimed to assess the effect of obesity on allergic inflammation and T helper-2 profile in an EoE experimental model. Methods: Obesity was induced by high-fat feeding. After 7¿weeks of diet, male BALB/c mice were subcutaneously sensitized and orally challenged with OVA. Results: Obesity itself induced a significant mast cell and eosinophil accumulation in the oesophagus, trachea, gut and lung. After allergy induction, this number was higher, when compared to lean-allergic mice. Moreover, obese-allergic mice showed higher remodelling area, in the oesophagus, associated with higher IL-5 and TSLP mRNA expression. In contrast, FoxP3 and IL-10 were less expressed in comparison with lean-allergic mice. In addition, the amount of CD11c+MHCII+PDL1+ dendritic cells was reduced, while the number of CD11c+MHCII+CD80+ DCs and CD3+CD4+GATA3+IL-4+ cells was increased in obese-allergic mice in the spleen and lymph nodes when compared to lean-allergic mice. Conclusion: Obesity aggravated the immune histopathological characteristics in the EoE experimental model, which was associated with the reduction in the regulatory profile, and the increased inflammatory cells influx, related to the TH2 profile. Altogether, the data provide new knowledge about obesity as a risk factor, worsening EoE symptoms, and contribute for future treatment strategies for this specific profile.

DOI 10.1111/cea.13533
Citations Scopus - 5Web of Science - 5
2019 Kulkarni G, de Waal K, Grahame S, Collison A, Roddick L, Hilton J, et al., 'Polysomnography for the management of oxygen supplementation therapy in infants with chronic lung disease of prematurity', Journal of Maternal-Fetal and Neonatal Medicine, 32 3640-3646 (2019) [C1]

© 2018, © 2018 Informa UK Limited, trading as Taylor &amp; Francis Group. Aim: Some infants with bronchopulmonary dysplasia (BPD) may require oxygen supplementation at home but ... [more]

© 2018, © 2018 Informa UK Limited, trading as Taylor & Francis Group. Aim: Some infants with bronchopulmonary dysplasia (BPD) may require oxygen supplementation at home but a role for overnight polysomnography (PSG) in the management of home oxygen therapy has been rarely described. Methods: Forty-one infants with BPD born at less than 30 weeks gestational age were discharged with continuous home oxygen supplementation therapy between 2010 and 2013. PSG data were recorded on oxygen supplementation versus room air at median corrected age of 2 months (range 1¿5 months) (first PSG after discharge to home). Those infants who continued oxygen supplementation therapy at home had at least one more PSG before oxygen therapy was discontinued (last PSG). We also collected PSG data in 10 healthy term infants (median age 3.5 months; range 2¿4 months). Results: In infants with BPD in room air, increased numbers of central apneas, hypopneas, and SaO2 desaturations were the predominant PSG features with a median apnea¿hypopnea index (AHI) of 16.8 events per hour (range 0¿155). On oxygen supplementation therapy, median AHI dramatically improved (2.2, range 0¿22; p <.001) and was not different from control infants (2.0, range 0¿3.9; p =.31). AHI on room air at the last PSG when home oxygen was ceased was 4.1 per hour (range 0¿13.8) slightly higher than in healthy infants. Conclusion: Central sleep disordered breathing in infants with BPD dramatically normalizes with low flow nasal cannula home oxygen therapy and improves with age. Mild central sleep disordered breathing remains detectable, although much improved, when compared with healthy infants at the time when the decision to cease home oxygen therapy was made by the physician.

DOI 10.1080/14767058.2018.1470234
Citations Scopus - 3Web of Science - 3
Co-authors Adam Collison
2019 Franklin D, Shellshear D, Babl FE, Schlapbach LJ, Oakley E, Borland ML, et al., 'Multicentre, randomised trial to investigate early nasal high-flow therapy in paediatric acute hypoxaemic respiratory failure: a protocol for a randomised controlled trial-a Paediatric Acute respiratory Intervention Study (PARIS 2)', BMJ OPEN, 9 (2019)
DOI 10.1136/bmjopen-2019-030516
2019 Mattes J, Gulliver T, Hilton J, Collison A, Whitehead B, 'Polysomnography in Preterm Infants with Bronchopulmonary Dysplasia for Monitoring Sleep-Disordered Breathing and Pulmonary Reserve', Current Sleep Medicine Reports, 5 56-60 (2019) [C1]

© 2019, Springer Nature Switzerland AG. Purpose of Review: Bronchopulmonary dysplasia (BPD) has progressed over time into a syndrome with multifactorial aetiology and complex path... [more]

© 2019, Springer Nature Switzerland AG. Purpose of Review: Bronchopulmonary dysplasia (BPD) has progressed over time into a syndrome with multifactorial aetiology and complex pathophysiology characterised by a developmental arrest of the alveolar and pulmonary vasculature compartments. BPD remains common in extremely preterm and very low birth weight infants. Maintaining appropriate oxygen blood levels in BPD infants may promote growth, reduce the risk of sudden infant death syndrome, and lower pulmonary artery pressures. There is no agreed approach on how to best titrate and wean home oxygen treatment in BPD infants. Recent Findings: In BPD infants on home oxygen therapy, sleep-disordered breathing is common and appears to be central in origin. However, obstructive apnoea events are also more common in BPD infants. The increased frequency of central apnoea events during sleep in BPD infants has been shown to decline on low-flow oxygen treatment to levels observed in healthy infants. It is hypothesised that brief respiratory pauses in sleep could result in significant oxygen desaturations in BPD infants who have a decreased pulmonary reserve. Those events are scored as central apnoea in polysomnography and are prevented by oxygen treatment. Central apnoea events may also represent disrupted control of breathing secondary to altered chemosensitivity. Summary: Polysomnography may be of clinical value to monitor sleep-disordered breathing, assess pulmonary reserves, and titrate and wean oxygen in BPD infants. Considering the increasing number of extremely preterm and very low birth weight infants with BPD, we recommend prioritising the performance of well-designed studies to gather high-level evidence into the potential role of polysomnography in the management of prematurity- and BPD-associated long-term sequelae.

DOI 10.1007/s40675-019-00141-2
Co-authors Adam Collison
2019 Bissell K, Ellwood P, Ellwood E, Chiang C-Y, Marks GB, El Sony A, et al., 'Essential Medicines at the National Level: The Global Asthma Network's Essential Asthma Medicines Survey 2014', INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH, 16 (2019) [C1]
DOI 10.3390/ijerph16040605
2019 Jensen ME, Murphy VE, Gibson PG, Mattes J, Camargo CA, 'Vitamin D status in pregnant women with asthma and its association with adverse respiratory outcomes during infancy', Journal of Maternal-Fetal and Neonatal Medicine, 32 1820-1825 (2019) [C1]

© 2018, © 2018 Informa UK Limited, trading as Taylor &amp; Francis Group. Background: Vitamin D may influence pregnancy and infant outcomes, especially infant respiratory health... [more]

© 2018, © 2018 Informa UK Limited, trading as Taylor & Francis Group. Background: Vitamin D may influence pregnancy and infant outcomes, especially infant respiratory health. This study aimed to examine vitamin D status in pregnant women with asthma, and whether higher vitamin D levels are associated with fewer adverse respiratory outcomes in their infants. Methods: Pregnant women with asthma, recruited from John Hunter Hospital Newcastle Australia (latitude 33°S), had serum total 25-hydroxyvitamin-D (25(OH)D) measured at 16 and 35 weeks gestation. Infant respiratory outcomes were collected at 12 months by parent-report questionnaire. Mother¿infant dyads were grouped by serum 25(OH)D during pregnancy: 25(OH)D < 75 nmol/L (at both time-points) versus 25(OH)D = 75 nmol/L (at one or both time-points). Results: In 52 pregnant women with asthma, mean serum 25(OH)D levels were 61 (range 26¿110) nmol/L at 16 weeks, and 65 (range 32¿116) nmol/L at 35 weeks, gestation. Thirty-one (60%) women had 25(OH)D < 75 nmol/L at both time-points; 21 (40%) had 25(OH)D = 75 nmol/L at one or both time-points. Maternal 25(OH)D < 75 nmol/L during pregnancy was associated with a higher proportion of infants with ¿wheeze ever¿ at 12 months, compared with 25(OH)D = 75 nmol/L (71 versus 43%, p =.04). Infant acute-care presentations (45 versus 13%, p =.02) and oral corticosteroid use (26 versus 4%, p =.03) due to ¿asthma/wheezing¿ were higher in the maternal group with 25(OH)D < 75 nmol/L, versus =75 nmol/L. Conclusions: Most pregnant women with asthma had low vitamin D status, which persisted across gestation. Low maternal vitamin D status was associated with greater risk of adverse respiratory outcomes in their infants, a group at high risk of developing childhood asthma.

DOI 10.1080/14767058.2017.1419176
Citations Scopus - 3Web of Science - 3
Co-authors Megan Jensen, Peter Gibson, Vanessa Murphy
2019 Collison AM, Li J, de Siqueira AP, Lv X, Toop HD, Morris JC, et al., 'TRAIL signals through the ubiquitin ligase MID1 to promote pulmonary fibrosis', BMC PULMONARY MEDICINE, 19 (2019) [C1]
DOI 10.1186/s12890-019-0786-x
Citations Scopus - 4Web of Science - 4
Co-authors Malcolm Starkey, Philip Hansbro, Adam Collison
2019 Nair PM, Starkey MR, Haw TJ, Liu G, Collison AM, Mattes J, et al., 'Enhancing tristetraprolin activity reduces the severity of cigarette smoke-induced experimental chronic obstructive pulmonary disease', CLINICAL & TRANSLATIONAL IMMUNOLOGY, 8 (2019) [C1]
DOI 10.1002/cti2.1084
Citations Scopus - 1
Co-authors Malcolm Starkey, Peter Wark, Nikki Verrills, Philip Hansbro, Adam Collison
2019 Robijn AL, Jensen ME, Gibson PG, Powell H, Giles WB, Clifton VL, et al., 'Trends in asthma self-management skills and inhaled corticosteroid use during pregnancy and postpartum from 2004 to 2017.', The Journal of asthma : official journal of the Association for the Care of Asthma, 56 594-602 (2019) [C1]
DOI 10.1080/02770903.2018.1471709
Citations Scopus - 5Web of Science - 5
Co-authors John Attia, Vanessa Murphy, Megan Jensen, Peter Gibson, Peter Wark
2018 Morten M, Collison A, Murphy VE, Barker D, Oldmeadow C, Attia J, et al., 'Managing Asthma in Pregnancy (MAP) trial: FENO levels and childhood asthma', Journal of Allergy and Clinical Immunology, 142 1765-1772.e4 (2018) [C1]

© 2018 American Academy of Allergy, Asthma &amp; Immunology Background: The single-center double-blind, randomized controlled Managing Asthma in Pregnancy (MAP) trial in Newcast... [more]

© 2018 American Academy of Allergy, Asthma & Immunology Background: The single-center double-blind, randomized controlled Managing Asthma in Pregnancy (MAP) trial in Newcastle, Australia, compared a treatment algorithm using the fraction of exhaled nitric oxide (FENO) in combination with asthma symptoms (FENO group) against a treatment algorithm using clinical symptoms only (clinical group) in pregnant asthmatic women (Australian New Zealand Clinical Trials Registry, no. 12607000561482). The primary outcome was a 50% reduction in asthma exacerbations during pregnancy in the FENO group. However, the effect of FENO-guided management on the development of asthma in the offspring is unknown. Objective: We sought to investigate the effect of FENO-guided asthma management during pregnancy on asthma incidence in childhood. Methods: A total of 179 mothers consented to participate in the Growing into Asthma (GIA) double-blind follow-up study with the primary aim to determine the effect of FENO-guided asthma management on childhood asthma incidence. Results: A total of 140 children (78%) were followed up at 4 to 6 years of age. FENO-guided as compared to symptoms-only approach significantly reduced doctor-diagnosed asthma (25.9% vs 43.2%; odds ratio [OR], 0.46, 95% CI, 0.22-0.96; P =.04). Furthermore, frequent wheeze (OR, 0.27; 95% CI, 0.09-0.87; P =.03), use of short-acting ß-agonists (OR, 0.49; 95% CI, 0.25-0.97; P =.04), and emergency department visits for asthma (OR, 0.17; 95% CI, 0.04-0.76; P =.02) in the past 12 months were less common in children born to mothers from the FENO group. Doctor-diagnosed asthma was associated with common risk alleles for early onset asthma at gene locus 17q21 (P =.01 for rs8069176; P =.03 for rs8076131), and higher airways resistance (P =.02) and FENO levels (P =.03). A causal mediation analysis suggested natural indirect effects of FENO-guided asthma management on childhood asthma through ¿any use¿ and ¿time to first change in dose¿ of inhaled corticosteroids during the MAP trial (OR: 0.83; 95% CI: 0.59-0.99, and OR: 0.90; 95% CI: 0.70-1.03, respectively). Conclusions: FENO-guided asthma management during pregnancy prevented doctor-diagnosed asthma in the offspring at preschool age, in part mediated through changes in use and dosing of inhaled corticosteroids during the MAP trial.

DOI 10.1016/j.jaci.2018.02.039
Citations Scopus - 20Web of Science - 19
Co-authors Peter Gibson, John Attia, Christopher Oldmeadow, Vanessa Murphy, Daniel Barker, Adam Collison
2017 Gould GS, Lim LL, Mattes J, 'Prevention and Treatment of Smoking and Tobacco Use During Pregnancy in Selected Indigenous Communities in High-Income Countries of the United States, Canada, Australia, and New Zealand: An Evidence-Based Review', Chest, 152 853-866 (2017) [C1]

© 2017 The Authors Tobacco smoking during pregnancy is the most important modifiable risk factor for adverse pregnancy outcomes and long-term health complications for mother and b... [more]

© 2017 The Authors Tobacco smoking during pregnancy is the most important modifiable risk factor for adverse pregnancy outcomes and long-term health complications for mother and baby. Tobacco use during pregnancy has decreased in high-income countries but not in Indigenous women in Australia, New Zealand, the United States, and Canada. This evidence-based review focuses on tobacco use among Indigenous pregnant women in high-income countries that share a history of European colonization. Indigenous women are more likely to use tobacco because of socioeconomic disadvantage, social norms, and poor access to culturally appropriate tobacco cessation support. Complications arising from tobacco smoking during pregnancy, such as low birth weight, prematurity, perinatal death, and sudden infant death syndrome, are much higher in Indigenous populations. Effective approaches to cessation in pregnant nonindigenous women involves behavioral counseling, with or without nicotine replacement therapy (NRT). Higher nicotine metabolism during pregnancy and poor adherence may affect therapeutic levels of NRT. Only two randomized trials were conducted among Indigenous women: neither found a statistically significant difference in cessation rates between the treatment and comparison arms. Considerations should be given to (1) whole life course approaches to reduce tobacco use in Indigenous women, (2) prohibiting tobacco promotion and reducing access to alcohol for minors to prevent smoking initiation in Indigenous youth, and (3) training health-care professionals in culturally appropriate smoking cessation care to improve access to services. It is critical to ensure acceptability and feasibility of study designs, consult with the relevant Indigenous communities, and preempt implementation challenges. Research is needed into the effect of reducing or stopping smoking during pregnancy when using NRT on subsequent maternal and infant outcomes.

DOI 10.1016/j.chest.2017.06.033
Citations Scopus - 10Web of Science - 7
Co-authors Gillian Gould
2017 Foster PS, Maltby S, Rosenberg HF, Tay HL, Hogan SP, Collison AM, et al., 'Modeling T

© 2017 John Wiley &amp; Sons A/S. Published by John Wiley &amp; Sons Ltd In this review, we highlight experiments conducted in our laboratories that have elucidated functional... [more]

© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd In this review, we highlight experiments conducted in our laboratories that have elucidated functional roles for CD4+ T-helper type-2 lymphocytes (TH2 cells), their associated cytokines, and eosinophils in the regulation of hallmark features of allergic asthma. Notably, we consider the complexity of type-2 responses and studies that have explored integrated signaling among classical TH2 cytokines (IL-4, IL-5, and IL-13), which together with CCL11 (eotaxin-1) regulate critical aspects of eosinophil recruitment, allergic inflammation, and airway hyper-responsiveness (AHR). Among our most important findings, we have provided evidence that the initiation of TH2 responses is regulated by airway epithelial cell-derived factors, including TRAIL and MID1, which promote TH2 cell development via STAT6-dependent pathways. Further, we highlight studies demonstrating that microRNAs are key regulators of allergic inflammation and potential targets for anti-inflammatory therapy. On the background of TH2 inflammation, we have demonstrated that innate immune cells (notably, airway macrophages) play essential roles in the generation of steroid-resistant inflammation and AHR secondary to allergen- and pathogen-induced exacerbations. Our work clearly indicates that understanding the diversity and spatiotemporal role of the inflammatory response and its interactions with resident airway cells is critical to advancing knowledge on asthma pathogenesis and the development of new therapeutic approaches.

DOI 10.1111/imr.12549
Citations Scopus - 40Web of Science - 34
Co-authors Hock Tay, Philip Hansbro, Ming Yang, Adam Collison, Gerard Kaiko, Steven Maltby, Nicole Hansbro, Paul Foster
2017 Kepreotes E, Whitehead B, Attia J, Oldmeadow C, Collison A, Searles A, et al., 'High-flow warm humidified oxygen versus standard low-flow nasal cannula oxygen for moderate bronchiolitis (HFWHO RCT): an open, phase 4, randomised controlled trial', The Lancet, 389 930-939 (2017) [C1]

© 2017 Elsevier Ltd Background Bronchiolitis is the most common lung infection in infants and treatment focuses on management of respiratory distress and hypoxia. High-flow warm h... [more]

© 2017 Elsevier Ltd Background Bronchiolitis is the most common lung infection in infants and treatment focuses on management of respiratory distress and hypoxia. High-flow warm humidified oxygen (HFWHO) is increasingly used, but has not been rigorously studied in randomised trials. We aimed to examine whether HFWHO provided enhanced respiratory support, thereby shortening time to weaning off oxygen. Methods In this open, phase 4, randomised controlled trial, we recruited children aged less than 24 months with moderate bronchiolitis attending the emergency department of the John Hunter Hospital or the medical unit of the John Hunter Children's Hospital in New South Wales, Australia. Patients were randomly allocated (1:1) via opaque sealed envelopes to HFWHO (maximum flow of 1 L/kg per min to a limit of 20 L/min using 1:1 air¿oxygen ratio, resulting in a maximum FiO2 of 0·6) or standard therapy (cold wall oxygen 100% via infant nasal cannulae at low flow to a maximum of 2 L/min) using a block size of four and stratifying for gestational age at birth. The primary outcome was time from randomisation to last use of oxygen therapy. All randomised children were included in the primary and secondary safety analyses. This trial is registered with the Australian New Zealand Clinical Trials Registry, number ACTRN12612000685819. Findings From July 16, 2012, to May 1, 2015, we randomly assigned 202 children to either HFWHO (101 children) or standard therapy (101 children). Median time to weaning was 24 h (95% CI 18¿28) for standard therapy and 20 h (95% CI 17¿34) for HFWHO (hazard ratio [HR] for difference in survival distributions 0·9 [95% CI 0·7¿1·2]; log rank p=0·61). Fewer children experienced treatment failure on HFWHO (14 [14%]) compared with standard therapy (33 [33%]; p=0·0016); of these children, those on HFWHO were supported for longer than were those on standard therapy before treatment failure (HR 0·3; 95% CI 0·2¿0·6; p<0·0001). 20 (61%) of 33 children who experienced treatment failure on standard therapy were rescued with HFWHO. 12 (12%) of children on standard therapy required transfer to the intensive care unit compared with 14 (14%) of those on HFWHO (difference -1%; 95% CI -7 to 16; p=0·41). Four adverse events occurred (oxygen desaturation and condensation inhalation in the HFWHO group, and two incidences of oxygen tubing disconnection in the standard therapy group); none resulted in withdrawal from the trial. No oxygen-related serious adverse events occurred. Secondary effectiveness outcomes are reported in the Results section. Interpretation HFWHO did not significantly reduce time on oxygen compared with standard therapy, suggesting that early use of HFWHO does not modify the underlying disease process in moderately severe bronchiolitis. HFWHO might have a role as a rescue therapy to reduce the proportion of children requiring high-cost intensive care. Funding Hunter Children's Research Foundation, John Hunter Hospital Charitable Trust, and the University of Newcastle Priority Research Centre GrowUpWell.

DOI 10.1016/S0140-6736(17)30061-2
Citations Scopus - 86Web of Science - 80
Co-authors John Attia, Adam Collison, Andrew Searles, Christopher Oldmeadow
2017 Le Fevre AK, Walker MM, Hadjiashrafy A, Bhatia R, Mattes J, Talley NJ, Nightingale S, 'Elevated Serum Tissue Transglutaminase Antibodies in Children With Eosinophilic Esophagitis.', Journal of pediatric gastroenterology and nutrition, 65 69-74 (2017)
DOI 10.1097/mpg.0000000000001437
Co-authors Nicholas Talley, Marjorie Walker
2017 Kim RY, Horvat JC, Pinkerton JW, Starkey MR, Essilfie AT, Mayall JR, et al., 'MicroRNA-21 drives severe, steroid-insensitive experimental asthma by amplifying phosphoinositide 3-kinase mediated suppression of histone deacetylase 2', Journal of Allergy and Clinical Immunology, 139 519-532 (2017) [C1]

© 2016 American Academy of Allergy, Asthma &amp; Immunology Background Severe steroid-insensitive asthma is a substantial clinical problem. Effective treatments are urgently req... [more]

© 2016 American Academy of Allergy, Asthma & Immunology Background Severe steroid-insensitive asthma is a substantial clinical problem. Effective treatments are urgently required, however, their development is hampered by a lack of understanding of the mechanisms of disease pathogenesis. Steroid-insensitive asthma is associated with respiratory tract infections and noneosinophilic endotypes, including neutrophilic forms of disease. However, steroid-insensitive patients with eosinophil-enriched inflammation have also been described. The¿mechanisms that underpin infection-induced, severe steroid-insensitive asthma can be elucidated by using mouse models of disease. Objective We sought to develop representative mouse models of severe, steroid-insensitive asthma and to use them to identify pathogenic mechanisms and investigate new treatment approaches. Methods Novel mouse models of Chlamydia, Haemophilus influenzae, influenza, and respiratory syncytial virus respiratory¿tract infections and ovalbumin-induced, severe, steroid-insensitive allergic airway disease (SSIAAD) in BALB/c mice were developed and interrogated. Results Infection induced increases in the levels of microRNA (miRNA)-21 (miR-21) expression in the lung during SSIAAD, whereas expression of the miR-21 target phosphatase and tensin homolog was reduced. This was associated with an increase in levels of phosphorylated Akt, an indicator of phosphoinositide 3-kinase (PI3K) activity, and decreased nuclear histone deacetylase (HDAC)2 levels. Treatment with an miR-21¿specific antagomir (Ant-21) increased phosphatase and tensin homolog levels. Treatment with Ant-21, or the pan-PI3K inhibitor LY294002, reduced PI3K activity and restored HDAC2 levels. This led to suppression of airway hyperresponsiveness and restored steroid sensitivity to allergic airway disease. These observations were replicated with SSIAAD associated with 4 different pathogens. Conclusion We identify a previously unrecognized role for an¿miR-21/PI3K/HDAC2 axis in SSIAAD. Our data highlight miR-21 as a novel therapeutic target for the treatment of this form of asthma.

DOI 10.1016/j.jaci.2016.04.038
Citations Scopus - 76Web of Science - 78
Co-authors Jay Horvat, Jemma Mayall, Malcolm Starkey, Philip Hansbro, Nicole Hansbro, Simon Keely, Paul Foster
2017 Girkin JL, Hatchwell LM, Collison AM, Starkey MR, Hansbro PM, Yagita H, et al., 'TRAIL signaling is proinflammatory and proviral in a murine model of rhinovirus 1B infection', American Journal of Physiology - Lung Cellular and Molecular Physiology, 312 L89-L99 (2017) [C1]

© 2017 the American Physiological Society. The aim of this study is to elucidate the role of TRAIL during rhinovirus (RV) infection in vivo. Naïve wild-type and tumor necrosis fac... [more]

© 2017 the American Physiological Society. The aim of this study is to elucidate the role of TRAIL during rhinovirus (RV) infection in vivo. Naïve wild-type and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-deficient (Tnfsf10-/-) BALB/c mice were infected intranasally with RV1B. In separate experiments, Tnfsf10-/-mice were sensitized and challenged via the airway route with house dust mite (HDM) to induce allergic airways disease and then challenged with RVIB or UV-RVIB. Airway hyperreactivity (AHR) was invasively assessed as total airways resistance in response to increasing methacholine challenge and inflammation was assessed in bronchoalveolar lavage fluid at multiple time points postinfection. Chemokines were quantified by ELISA of whole lung lysates and viral load was determined by quantitative RT-PCR and tissue culture infective dose (TCID50). Human airway epithelial cells (BEAS2B) were infected with RV1B and stimulated with recombinant TRAIL or neutralizing anti-TRAIL antibodies and viral titer assessed by TCID50. HDM-challenged Tnfsf10-/-mice were protected against RV-induced AHR and had suppressed cellular infiltration in the airways upon RV infection. Chemokine C-X-C-motif ligand 2 (CXCL2) production was suppressed in naïve Tnfsf10-/-mice infected with RV1B, with less RV1B detected 24 h postinfection. This was associated with reduced apoptotic cell death and a reduction of interferon (IFN)-¿2/3 but not IFN-a or IFN-ß. TRAIL stimulation increased, whereas anti-TRAIL antibodies reduced viral replication in RV1B-infected BEAS2B cells in vitro. In conclusion, TRAIL promotes RV-induced AHR, inflammation and RV1B replication, implicating this molecule and its downstream signaling pathways as a possible target for the amelioration of RV1B-induced allergic and nonallergic lung inflammation and AHR.

DOI 10.1152/ajplung.00200.2016
Citations Scopus - 9Web of Science - 9
Co-authors Jason Girkin, Adam Collison, Malcolm Starkey, Paul Foster, Philip Hansbro
2017 Le Fevre AK, Walker MM, Hadjiashrafy A, Bhatia R, Mattes J, Talley NJ, Nightingale S, 'Elevated Serum Tissue Transglutaminase Antibodies in Children With Eosinophilic Esophagitis.', Journal of pediatric gastroenterology and nutrition, 65 69-74 (2017) [C1]
DOI 10.1097/mpg.0000000000001437
Citations Scopus - 3Web of Science - 3
Co-authors Marjorie Walker, Nicholas Talley
2017 Asher I, Haahtela T, Selroos O, Ellwood P, Ellwood E, Billo NE, et al., 'Global Asthma Network survey suggests more national asthma strategies could reduce burden of asthma', Allergologia et Immunopathologia, 45 105-114 (2017)

© 2017 SEICAP Background Several countries or regions within countries have an effective national asthma strategy resulting in a reduction of the large burden of asthma to individ... [more]

© 2017 SEICAP Background Several countries or regions within countries have an effective national asthma strategy resulting in a reduction of the large burden of asthma to individuals and society. There has been no systematic appraisal of the extent of national asthma strategies in the world. Methods The Global Asthma Network (GAN) undertook an email survey of 276 Principal Investigators of GAN centres in 120 countries, in 2013¿2014. One of the questions was: ¿Has a national asthma strategy been developed in your country for the next five years? For children? For adults?¿. Results Investigators in 112 (93.3%) countries answered this question. Of these, 26 (23.2%) reported having a national asthma strategy for children and 24 (21.4%) for adults; 22 (19.6%) countries had a strategy for both children and adults; 28 (25%) had a strategy for at least one age group. In countries with a high prevalence of current wheeze, strategies were significantly more common than in low prevalence countries (11/13 (85%) and 7/31 (22.6%) respectively, p¿<¿0.001). Interpretation In 25% countries a national asthma strategy was reported. A large reduction in the global burden of asthma could be potentially achieved if more countries had an effective asthma strategy.

DOI 10.1016/j.aller.2016.10.013
Citations Scopus - 9
2017 Dunn A, Pearce K, Callister R, Collison A, Morten M, Mandaliya P, et al., 'Exercise capacity is not decreased in children who have undergone lung resection early in life for congenital thoracic malformations compared to healthy age-matched children', Pediatric Pulmonology, 52 1340-1348 (2017) [C1]

© 2017 Wiley Periodicals, Inc. Purpose: The purpose of this study was to compare (i) the exercise capacity and (ii) lung function prior to and immediately post cardiopulmonary exe... [more]

© 2017 Wiley Periodicals, Inc. Purpose: The purpose of this study was to compare (i) the exercise capacity and (ii) lung function prior to and immediately post cardiopulmonary exercise tests (CPET) of children who underwent early life lung resection for Congenital Pulmonary Airway Malformations (CPAM) to healthy control children. Method: Eight children with CPAM (four males, age 9.6 ± 1.8 years) and eight control children without respiratory disease (three males, age 9.4 ± 1.4 years) performed a CPET on a cycle ergometer, during which maximal oxygen consumption (V¿O2max) and heart rate were measured. Prior to and immediately post CPET, lung function measures including Nitrogen Multiple Breath Washout (MBW) and spirometry were performed. Results: There were no significant between group differences in pre CPET lung function (P > 0.05) or maximal exercise capacity (V¿O2max CPAM: 39.4 mL.kg-1.min-1, Control: 40.5 mL.kg-1.min-1). Post CPET, FEV1 was significantly lower in the CPAM group, with two participants diagnosed subsequently with exercise induced bronchospasm based on post-CPET spirometry and follow-up clinical investigations. Conclusion: Early life lung resection for CPAM does not appear to have negative implications for exercise capacity later in childhood. Clinicians should be aware that dyspnoea following exercise may be due to asthma rather than residual effects of CPAM in these children.

DOI 10.1002/ppul.23772
Citations Scopus - 3Web of Science - 3
Co-authors Ben Dascombe, Robin Callister, Adam Collison
2017 Silva FMC, Oliveira EE, Gouveia ACC, Brugiolo ASS, Alves CC, Correa JOA, et al., 'Obesity promotes prolonged ovalbumin-induced airway inflammation modulating T helper type 1 (Th1), Th2 and Th17 immune responses in BALB/c mice', Clinical and Experimental Immunology, 189 47-59 (2017) [C1]

© 2017 British Society for Immunology Clinical and epidemiological studies indicate that obesity affects the development and phenotype of asthma by inducing inflammatory mechanism... [more]

© 2017 British Society for Immunology Clinical and epidemiological studies indicate that obesity affects the development and phenotype of asthma by inducing inflammatory mechanisms in addition to eosinophilic inflammation. The aim of this study was to assess the effect of obesity on allergic airway inflammation and T helper type 2 (Th2) immune responses using an experimental model of asthma in BALB/c mice. Mice fed a high-fat diet (HFD) for 10 weeks were sensitized and challenged with ovalbumin (OVA), and analyses were performed at 24 and 48 h after the last OVA challenge. Obesity induced an increase of inducible nitric oxide synthase (iNOS)-expressing macrophages and neutrophils which peaked at 48 h after the last OVA challenge, and was associated with higher levels of interleukin (IL)-4, IL-9, IL-17A, leptin and interferon (IFN)-¿ in the lungs. Higher goblet cell hyperplasia was associated with elevated mast cell influx into the lungs and trachea in the obese allergic mice. In contrast, early eosinophil influx and lower levels of IL-25, thymic stromal lymphopoietin (TSLP), CCL11 and OVA-specific immunoglobulin (IgE) were observed in the obese allergic mice in comparison to non-obese allergic mice. Moreover, obese mice showed higher numbers of mast cells regardless of OVA challenge. These results indicate that obesity affects allergic airway inflammation through mechanisms involving mast cell influx and the release of TSLP and IL-25, which favoured a delayed immune response with an exacerbated Th1, Th2 and Th17 profile. In this scenario, an intense mixed inflammatory granulocyte influx, classically activated macrophage accumulation and intense mucus production may contribute to a refractory therapeutic response and exacerbate asthma severity.

DOI 10.1111/cei.12958
Citations Scopus - 20Web of Science - 19
2016 Sokulsky LA, Collison AM, Nightingale S, Le Fevre A, Percival E, Starkey MR, et al., 'TRAIL deficiency and PP2A activation with salmeterol ameliorates egg allergen-driven eosinophilic esophagitis', American Journal of Physiology - Gastrointestinal and Liver Physiology, 311 G998-G1008 (2016) [C1]

© 2016 the American Physiological Society. Food antigens are common inflammatory triggers in pediatric eosinophilic esophagitis (EoE). TNFrelated apoptosis-inducing ligand (TRAIL)... [more]

© 2016 the American Physiological Society. Food antigens are common inflammatory triggers in pediatric eosinophilic esophagitis (EoE). TNFrelated apoptosis-inducing ligand (TRAIL) promotes eosinophilic inflammation through the upregulation of the E3 ubiquitin ligase Midline (MID)-1 and subsequent downregulation of protein phosphatase 2A (PP2A), but the role of this pathway in EoE that is experimentally induced by repeated food antigen challenges has not been investigated. Esophageal mucosal biopsies were collected from children with EoE and controls and assessed for TRAIL and MID-1 protein and mRNA transcript levels. Wild-type and TRAIL-deficient (Tnfsf10-/-) mice were administered subcutaneous ovalbumin (OVA) followed by oral OVA challenges. In separate experiments, OVA-challenged mice were intraperitoneally administered salmeterol or dexamethasone. Esophageal biopsies from children with EoE revealed increased levels of TRAIL and MID-1 and reduced PP2A activation compared with controls. Tnfsf10-/- mice were largely protected from esophageal fibrosis, eosinophilic inflammation, and the upregulation of TSLP, IL-5, IL-13, and CCL11 when compared with wild-type mice. Salmeterol administration to wild-type mice with experimental EoE restored PP2A activity and also prevented esophageal eosinophilia, inflammatory cytokine expression, and remodeling, which was comparable to the treatment effect of dexamethasone. TRAIL and PP2A regulate inflammation and fibrosis in experimental EoE, which can be therapeutically modulated by salmeterol.

DOI 10.1152/ajpgi.00151.2016
Citations Scopus - 7Web of Science - 6
Co-authors Adam Collison, Malcolm Starkey, Philip Hansbro, Paul Foster
2016 Woolard A, Benders T, Campbell L, Karayanidis F, Mattes J, Murphy V, et al., 'Exploring the association of infant temperament on maternal fundamental frequency contours', Sixteenth Australasian International Conference on Speech Science and Technology, 229-232 (2016)
Co-authors Frini Karayanidis, Vanessa Murphy, Alix Woolard Uon, Alison Lane, Linda E Campbell
2016 Haw TJ, Starkey MR, Nair PM, Pavlidis S, Liu G, Nguyen DH, et al., 'A pathogenic role for tumor necrosis factor-related apoptosis-inducing ligand in chronic obstructive pulmonary disease', Mucosal Immunology, 9 859-872 (2016) [C1]

Chronic obstructive pulmonary disease (COPD) is a life-Threatening inflammatory respiratory disorder, often induced by cigarette smoke (CS) exposure. The development of effective ... [more]

Chronic obstructive pulmonary disease (COPD) is a life-Threatening inflammatory respiratory disorder, often induced by cigarette smoke (CS) exposure. The development of effective therapies is impaired by a lack of understanding of the underlining mechanisms. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a cytokine with inflammatory and apoptotic properties. We interrogated a mouse model of CS-induced experimental COPD and human tissues to identify a novel role for TRAIL in COPD pathogenesis. CS exposure of wild-Type mice increased TRAIL and its receptor messenger RNA (mRNA) expression and protein levels, as well as the number of TRAIL + CD11b + monocytes in the lung. TRAIL and its receptor mRNA were also increased in human COPD. CS-exposed TRAIL-deficient mice had decreased pulmonary inflammation, pro-inflammatory mediators, emphysema-like alveolar enlargement, and improved lung function. TRAIL-deficient mice also developed spontaneous small airway changes with increased epithelial cell thickness and collagen deposition, independent of CS exposure. Importantly, therapeutic neutralization of TRAIL, after the establishment of early-stage experimental COPD, reduced pulmonary inflammation, emphysema-like alveolar enlargement, and small airway changes. These data provide further evidence for TRAIL being a pivotal inflammatory factor in respiratory diseases, and the first preclinical evidence to suggest that therapeutic agents that target TRAIL may be effective in COPD therapy.

DOI 10.1038/mi.2015.111
Citations Scopus - 29Web of Science - 30
Co-authors Darryl Knight, Peter Wark, Jay Horvat, Malcolm Starkey, Philip Hansbro, Alan Hsu, Paul Foster, Adam Collison
2016 Maltby S, Gibson P, Mattes J, McDonald VM, 'How to treat Severe Asthma Part 2 Management.', Australian Doctor, (2016)
Co-authors Steven Maltby, Vanessa Mcdonald, Peter Gibson
2016 Maltby S, Gibson P, Mattes J, McDonald VM, 'How to treat Severe Asthma Part 1 Diagnosis', Australian Doctor, (2016)
Co-authors Vanessa Mcdonald, Steven Maltby, Peter Gibson
2016 Lum S, Bountziouka V, Wade A, Hoo AF, Kirkby J, Moreno-Galdo A, et al., 'New reference ranges for interpreting forced expiratory manoeuvres in infants and implications for clinical interpretation: A multicentre collaboration', Thorax, 71 276-283 (2016) [C1]

The raised volume rapid thoracoabdominal compression (RVRTC) technique is commonly used to obtain full forced expiratory manoeuvres from infants, but reference equations derived f... [more]

The raised volume rapid thoracoabdominal compression (RVRTC) technique is commonly used to obtain full forced expiratory manoeuvres from infants, but reference equations derived from 'in-house' equipment have been shown to be inappropriate for current commercially available devices. Aim: To explore the impact of equipment differences on RVRTC outcomes, derive robust equipment-specific RVRTC reference ranges and investigate their potential clinical impact on data interpretation. Method: RVRTC data from healthy subjects using Jaeger BabyBody or the 'Respiratory Analysis Software Program, RASP' systems were collated from four centres internationally. Data were excluded if gestational age <37 weeks or birth weight <2.5 kg. Reference equations for RVRTC outcomes were constructed using the LMS (lambda-mu-sigma) method, and compared with published equations using data from newborn screened infants with cystic fibrosis (CF). Results: RVRTC data from 429 healthy infants (50.3% boys; 88% white infants) on 639 occasions aged 4-118 weeks were available. When plotted against length, flows were significantly higher with RASP than Jaeger, requiring construction of separate equipment-specific regression equations. When comparing results derived from the new equations with those from widely used published equations based on different equipments, discrepancies in forced expiratory volumes and flows of up to 2.5 z-scores were observed, the magnitude of which increased with age. According to published equations, 25% of infants with CF fell below the 95% limits of normal for FEV0.5, compared with only 10% when using the new equations. Conclusions: Use of equipment-specific prediction equations for RVRTC outcomes will enhance interpretation of infant lung function results; particularly during longitudinal follow-up.

DOI 10.1136/thoraxjnl-2015-207278
Citations Scopus - 17Web of Science - 17
2016 Murphy VE, Jensen ME, Mattes J, Hensley MJ, Giles WB, Peek MJ, et al., 'The Breathing for Life Trial: a randomised controlled trial of fractional exhaled nitric oxide (FENO)-based management of asthma during pregnancy and its impact on perinatal outcomes and infant and childhood respiratory health', BMC PREGNANCY AND CHILDBIRTH, 16 (2016)
DOI 10.1186/s12884-016-0890-3
Citations Scopus - 17Web of Science - 16
Co-authors Vanessa Murphy, Michael Hensley, John Attia, Andrew Searles, Megan Jensen, Peter Gibson
2016 Searles A, Doran C, Attia J, Knight D, Wiggers J, Deeming S, et al., 'An approach to measuring and encouraging research translation and research impact', HEALTH RESEARCH POLICY AND SYSTEMS, 14 (2016) [C1]
DOI 10.1186/s12961-016-0131-2
Citations Scopus - 26Web of Science - 29
Co-authors Rod Ling, John Wiggers, Michael Nilsson, Darryl Knight, John Attia, Andrew Searles
2016 Judd LM, Heine RG, Menheniott TR, Buzzelli J, O Brien-Simpson N, Pavlic D, et al., 'Elevated IL-33 expression is associated with pediatric eosinophilic esophagitis, and exogenous IL-33 promotes eosinophilic esophagitis development in mice', American Journal of Physiology - Gastrointestinal and Liver Physiology, 310 G13-G25 (2016) [C1]

© 2016 the American Physiological Society. We tested whether the T helper (Th) type 2 (Th2) cell agonist and allergenic ligand IL-33 was associated with eosinophilic esophagitis (... [more]

© 2016 the American Physiological Society. We tested whether the T helper (Th) type 2 (Th2) cell agonist and allergenic ligand IL-33 was associated with eosinophilic esophagitis (EoE) development in a pediatric cohort and whether IL-33 protein could induce disease symptoms in mice. Biopsies from EoE patients or controls were used to measure IL-33 mRNA and protein expression. Increased expression of IL-33 mRNA was found in the esophageal mucosa in EoE. IL-33 protein was detected in cells negative for CD45, mast cells, and epithelial cell markers near blood vessels. Circulating levels of IL-33 were not increased. The time course for IL-33 gene expression was quantified in an established Aspergillus fumigatus allergen mouse model of EoE. Because IL-33 induction was transient in this model and chronicity of IL-33 expression has been demonstrated in humans, naive mice were treated with recombinant IL-33 for 1 wk and esophageal pathology was evaluated. IL-33 application produced changes consistent with phenotypically early EoE, including transmural eosinophilia, mucosal hyperproliferation, and upregulation of eosinophilic genes and chemokines. Th2 cytokines, including IL-13, along with innate lymphoid cell group 2, Th1/17, and M2 macrophage marker genes, were increased after IL-33 application. IL-33-induced eosinophilia was ablated in IL-13 null mice. In addition, IL-33 induced a profound inhibition of the regulatory T cell gene signature. We conclude that IL-33 gene expression is associated with pediatric EoE development and that application of recombinant protein in mice phenocopies the early clinical phase of the human disease in an IL-13-dependent manner. IL-33 inhibition of esophageal regulatory T cell function may induce loss of antigenic tolerance, thereby providing a mechanistic rationale for EoE development.

DOI 10.1152/ajpgi.00290.2015
Citations Scopus - 27Web of Science - 24
Co-authors Adam Collison
2016 Lovett S, Roche J, Hunter S, Symonds I, Tomlinson N, Gagnon R, et al., 'Respective value of the traditional clinical rotation and high fidelity simulation on the acquisition of clinical reasoning skills in medical students A Randomized Controlled Trial.', MedEdPublish, 5 (2016) [C1]
DOI 10.15694/mep.2016.000037
Co-authors Ian Symonds, Sharyn Hunter
2016 Percival E, Bhatia R, Preece K, McElduff P, McEvoy M, Collison A, Mattes J, 'Reproducibility of serum IgE, Ara h2 skin prick testing and fraction of exhaled nitric oxide for predicting clinical peanut allergy in children', ALLERGY ASTHMA AND CLINICAL IMMUNOLOGY, 12 (2016) [C1]
DOI 10.1186/s13223-016-0143-z
Citations Scopus - 1Web of Science - 2
Co-authors Mark Mcevoy, Adam Collison, Patrick Mcelduff
2015 Thorburn AN, McKenzie CI, Shen S, Stanley D, MacIa L, Mason LJ, et al., 'Evidence that asthma is a developmental origin disease influenced by maternal diet and bacterial metabolites', Nature Communications, 6 (2015) [C1]

© 2015 Macmillan Publishers Limited. All rights reserved. Asthma is prevalent in Western countries, and recent explanations have evoked the actions of the gut microbiota. Here we ... [more]

© 2015 Macmillan Publishers Limited. All rights reserved. Asthma is prevalent in Western countries, and recent explanations have evoked the actions of the gut microbiota. Here we show that feeding mice a high-fibre diet yields a distinctive gut microbiota, which increases the levels of the short-chain fatty acid, acetate. High-fibre or acetate-feeding led to marked suppression of allergic airways disease (AAD, a model for human asthma), by enhancing T-regulatory cell numbers and function. Acetate increases acetylation at the Foxp3 promoter, likely through HDAC9 inhibition. Epigenetic effects of fibre/acetate in adult mice led us to examine the influence of maternal intake of fibre/acetate. High-fibre/acetate feeding of pregnant mice imparts on their adult offspring an inability to develop robust AAD. High fibre/acetate suppresses expression of certain genes in the mouse fetal lung linked to both human asthma and mouse AAD. Thus, diet acting on the gut microbiota profoundly influences airway responses, and may represent an approach to prevent asthma, including during pregnancy.

DOI 10.1038/ncomms8320
Citations Scopus - 308Web of Science - 298
Co-authors Lisa Wood, Vanessa Murphy, Peter Gibson
2015 Tay HL, Kaiko GE, Plank M, Li J, Maltby S, Essilfie A-T, et al., 'Correction: Antagonism of miR-328 Increases the Antimicrobial Function of Macrophages and Neutrophils and Rapid Clearance of Non-typeable Haemophilus Influenzae (NTHi) from Infected Lung.', PLoS pathogens, 11 e1004956 (2015) [O1]
DOI 10.1371/journal.ppat.1004956
Citations Scopus - 2
Co-authors Gerard Kaiko, Ming Yang, Philip Hansbro, Hock Tay, Steven Maltby, Paul Foster
2015 Collison AM, Sokulsky LA, Sherrill JD, Nightingale S, Hatchwell L, Talley NJ, et al., 'TNF-related apoptosis-inducing ligand (TRAIL) regulates midline-1, thymic stromal lymphopoietin, inflammation, and remodeling in experimental eosinophilic esophagitis', Journal of Allergy and Clinical Immunology, 136 971-982 (2015) [C1]

© 2015 American Academy of Allergy, Asthma &amp; Immunology. Background Eosinophilic esophagitis (EoE) is an inflammatory disorder of the esophagus defined by eosinophil infiltr... [more]

© 2015 American Academy of Allergy, Asthma & Immunology. Background Eosinophilic esophagitis (EoE) is an inflammatory disorder of the esophagus defined by eosinophil infiltration and tissue remodeling with resulting symptoms of esophageal dysfunction. TNF-related apoptosis-inducing ligand (TRAIL) promotes inflammation through upregulation of the E3 ubiquitin-ligase midline-1 (MID1), which binds to and deactivates the catalytic subunit of protein phosphatase 2Ac, resulting in increased nuclear factor ¿B activation. Objective We sought to elucidate the role of TRAIL in EoE. Methods We used Aspergillus fumigatus to induce EoE in TRAIL-sufficient (wild-type) and TRAIL-deficient (TRAIL-/-) mice and targeted MID1 in the esophagus with small interfering RNA. We also treated mice with recombinant thymic stromal lymphopoietin (TSLP) and TRAIL. Results TRAIL deficiency and MID1 silencing with small interfering RNA reduced esophageal eosinophil and mast cell numbers and protected against esophageal circumference enlargement, muscularis externa thickening, and collagen deposition. MID1 expression and nuclear factor ¿B activation were reduced in TRAIL-/- mice, whereas protein phosphatase 2Ac levels were increased compared with those seen in wild-type control mice. This was associated with reduced expression of CCL24, CCL11, CCL20, IL-5, IL-13, IL-25, TGFB, and TSLP. Treatment with TSLP reconstituted hallmark features of EoE in TRAIL-/- mice and recombinant TRAIL induced esophageal TSLP expression in vivo in the absence of allergen. Post hoc analysis of gene array data demonstrated significant upregulation of TRAIL and MID1 in a cohort of children with EoE compared with that seen in controls. Conclusion TRAIL regulates MID1 and TSLP, inflammation, fibrosis, smooth muscle hypertrophy, and expression of inflammatory effector chemokines and cytokines in experimental EoE.

DOI 10.1016/j.jaci.2015.03.031
Citations Scopus - 16Web of Science - 13
Co-authors Adam Collison, Nicholas Talley, Marjorie Walker
2015 Schilter HC, Collison A, Russo RC, Foot JS, Yow TT, Vieira AT, et al., 'Effects of an anti-inflammatory VAP-1/SSAO inhibitor, PXS-4728A, on pulmonary neutrophil migration', Respiratory Research, 16 (2015) [C1]

© Schilter et al. Background and purpose: The persistent influx of neutrophils into the lung and subsequent tissue damage are characteristics of COPD, cystic fibrosis and acute lu... [more]

© Schilter et al. Background and purpose: The persistent influx of neutrophils into the lung and subsequent tissue damage are characteristics of COPD, cystic fibrosis and acute lung inflammation. VAP-1/SSAO is an endothelial bound adhesion molecule with amine oxidase activity that is reported to be involved in neutrophil egress from the microvasculature during inflammation. This study explored the role of VAP-1/SSAO in neutrophilic lung mediated diseases and examined the therapeutic potential of the selective inhibitor PXS-4728A. Methods: Mice treated with PXS-4728A underwent intra-vital microscopy visualization of the cremaster muscle upon CXCL1/KC stimulation. LPS inflammation, Klebsiella pneumoniae infection, cecal ligation and puncture as well as rhinovirus exacerbated asthma models were also assessed using PXS-4728A. Results: Selective VAP-1/SSAO inhibition by PXS-4728A diminished leukocyte rolling and adherence induced by CXCL1/KC. Inhibition of VAP-1/SSAO also dampened the migration of neutrophils to the lungs in response to LPS, Klebsiella pneumoniae lung infection and CLP induced sepsis; whilst still allowing for normal neutrophil defense function, resulting in increased survival. The functional effects of this inhibition were demonstrated in the RV exacerbated asthma model, with a reduction in cellular infiltrate correlating with a reduction in airways hyperractivity. Conclusions and implications: This study demonstrates that the endothelial cell ligand VAP-1/SSAO contributes to the migration of neutrophils during acute lung inflammation, pulmonary infection and airway hyperractivity. These results highlight the potential of inhibiting of VAP-1/SSAO enzymatic function, by PXS-4728A, as a novel therapeutic approach in lung diseases that are characterized by neutrophilic pattern of inflammation.

DOI 10.1186/s12931-015-0200-z
Citations Scopus - 32Web of Science - 31
Co-authors Adam Collison
2015 Li JJ, Tay HL, Maltby S, Xiang Y, Eyers F, Hatchwell L, et al., 'MicroRNA-9 regulates steroid-resistant airway hyperresponsiveness by reducing protein phosphatase 2A activity', Journal of Allergy and Clinical Immunology, 136 462-473 (2015) [C1]

© 2015 American Academy of Allergy, Asthma &amp; Immunology. Background Steroid-resistant asthma is a major clinical problem that is linked to activation of innate immune cells.... [more]

© 2015 American Academy of Allergy, Asthma & Immunology. Background Steroid-resistant asthma is a major clinical problem that is linked to activation of innate immune cells. Levels of IFN-¿ and LPS are often increased in these patients. Cooperative signaling between IFN-¿/LPS induces macrophage-dependent steroid-resistant airway hyperresponsiveness (AHR) in mouse models. MicroRNAs (miRs) are small noncoding RNAs that regulate the function of innate immune cells by controlling mRNA stability and translation. Their role in regulating glucocorticoid responsiveness and AHR remains unexplored. Objective IFN-¿ and LPS synergistically increase the expression of miR-9 in macrophages and lung tissue, suggesting a role in the mechanisms of steroid resistance. Here we demonstrate the role of miR-9 in IFN-¿/LPS-induced inhibition of dexamethasone (DEX) signaling in macrophages and in induction of steroid-resistant AHR. Methods MiRNA-9 expression was assessed by means of quantitative RT-PCR. Putative miR-9 targets were determined in silico and confirmed in luciferase reporter assays. miR-9 function was inhibited with sequence-specific antagomirs. The efficacy of DEX was assessed by quantifying glucocorticoid receptor (GR) cellular localization, protein phosphatase 2A (PP2A) activity, and AHR. Results Exposure of pulmonary macrophages to IFN-¿/LPS synergistically induced miR-9 expression; reduced levels of its target transcript, protein phosphatase 2 regulatory subunit B (B56) d isoform; attenuated PP2A activity; and inhibited DEX-induced GR nuclear translocation. Inhibition of miR-9 increased both PP2A activity and GR nuclear translocation in macrophages and restored steroid sensitivity in multiple models of steroid-resistant AHR. Pharmacologic activation of PP2A restored DEX efficacy and inhibited AHR. MiR-9 expression was increased in sputum of patients with neutrophilic but not those with eosinophilic asthma. Conclusion MiR-9 regulates GR signaling and steroid-resistant AHR. Targeting miR-9 function might be a novel approach for the treatment of steroid-resistant asthma.

DOI 10.1016/j.jaci.2014.11.044
Citations Scopus - 49Web of Science - 49
Co-authors Hock Tay, Paul Foster, Steven Maltby, Ming Yang
2015 Hatchwell L, Collison A, Girkin J, Parsons K, Li J, Zhang J, et al., 'Toll-like receptor 7 governs interferon and inflammatory responses to rhinovirus and is suppressed by IL-5-induced lung eosinophilia', Thorax, (2015) [C1]

© 2015 BMJ Publishing Group Ltd &amp; British Thoracic Society.Background Asthma exacerbations represent a significant disease burden and are commonly caused by rhinovirus (RV), w... [more]

© 2015 BMJ Publishing Group Ltd & British Thoracic Society.Background Asthma exacerbations represent a significant disease burden and are commonly caused by rhinovirus (RV), which is sensed by Toll-like receptors (TLR) such as TLR7. Some asthmatics have impaired interferon (IFN) responses to RV, but the underlying mechanisms of this clinically relevant observation are poorly understood. Objectives To investigate the importance of intact TLR7 signalling in vivo during RV exacerbation using mouse models of house dust mite (HDM)-induced allergic airways disease exacerbated by a superimposed RV infection. Methods Wild-type and TLR7-deficient (Tlr7<sup>-/-</sup>) BALB/c mice were intranasally sensitised and challenged with HDM prior to infection with RV1B. In some experiments, mice were administered recombinant IFN or adoptively transferred with plasmacytoid dendritic cells (pDC). Results Allergic Tlr7<sup>-/-</sup> mice displayed impaired IFN release upon RV1B infection, increased virus replication and exaggerated eosinophilic inflammation and airways hyper reactivity. Treatment with exogenous IFN or adoptive transfer of TLR7-competent pDCs blocked these exaggerated inflammatory responses and boosted IFN? release in the absence of host TLR7 signalling. TLR7 expression in the lungs was suppressed by allergic inflammation and by interleukin (IL)-5-induced eosinophilia in the absence of allergy. Subjects with moderate-to-severe asthma and eosinophilic but not neutrophilic airways inflammation, despite inhaled steroids, showed reduced TLR7 and IFN?2/3 expression in endobronchial biopsies. Furthermore, TLR7 expression inversely correlated with percentage of sputum eosinophils. Conclusions This implicates IL-5-induced airways eosinophilia as a negative regulator of TLR7 expression and antiviral responses, which provides a molecular mechanism underpinning the effect of eosinophil-targeting treatments for the prevention of asthma exacerbations.

DOI 10.1136/thoraxjnl-2014-205465
Citations Scopus - 52Web of Science - 49
Co-authors Jason Girkin, Peter Wark, Paul Foster, Nathan Bartlett, Adam Collison, Darryl Knight
2015 Mandaliya PH, Morten M, Kumar R, James A, Deshpande A, Murphy VE, et al., 'Ventilation inhomogeneities in children with congenital thoracic malformations', BMC Pulmonary Medicine, 15 (2015) [C1]

© Morten et al.; licensee BioMed Central. Background: Congenital thoracic malformations (CTM) are rare lung lesions that are managed with surgical resection or active surveillance... [more]

© Morten et al.; licensee BioMed Central. Background: Congenital thoracic malformations (CTM) are rare lung lesions that are managed with surgical resection or active surveillance. Methods: Nitrogen lung clearance index (LCI), reactance and resistance (X5Hz and R5Hz), forced expiratory volume in 1 s and forced vital capacity (FEV1 and FVC) were prospectively measured in 10 children with CTM (mean age/SD: 7.6/1.3) who had undergone surgical resection in early life and in 17 healthy children (mean age/SD: 4.8/0.4). Total lung capacity (TLC) was also conducted in children older than 7 years of age with CTM (n = 8). Results: Mean LCI was 8.0 (95% CI 7.5 to 8.5) in the CTM group and 7.3 (95% CI 7.0 to 7.6) in healthy children (p = 0.016). Mean X5Hz was -0.44kPa/l/s (95% CI -0.58 to -0.31) in the CTM group and -0.31kPa/l/s (95% CI -0.35 to -0.27) in healthy children (p = 0.02). Mean Z score for X5Hz was -2.11 (95% CI -3.59 to -0.63) in the CTM group and -0.11 (95% CI -0.55 to 0.33) in healthy children (p = 0.0008). Mean FEV1 was 1.21 L (95% CI 0.97 to 1.45) in the CTM group and 1.02 L (95% CI 0.90 to 1.15) in healthy children (p = 0.22). Mean % predicted FEV1 was 83% (95% CI 74 to 92) in the CTM group and 97% (95% CI 87 to 107) in healthy children (p < 0.05). Mean % predicted TLC in CTM children was 121.3% (95% CI 88.45 to 154.1). Mean LCI was inversely correlated with height z-scores in the CTM group (rs = -0.88, p = 0.002) but not in healthy children (rs = 0.22, p = 0.4). Conclusions: Children with CTM have impaired lung function as demonstrated by the significant differences in LCI, reactance and FEV1 but not FVC, resistance and TLC. These findings may be of clinical relevance as ventilation inhomogeneities are closely correlated with somatic growth in this study.

DOI 10.1186/s12890-015-0023-1
Citations Scopus - 4Web of Science - 5
Co-authors Peter Gibson, Vanessa Murphy, Aniruddh Deshpande
2015 Girkin J, Hatchwell L, Foster P, Johnston SL, Bartlett N, Collison A, Mattes J, 'CCL7 and IRF-7 mediate hallmark inflammatory and IFN responses following rhinovirus 1B infection', Journal of Immunology, 194 4924-4930 (2015) [C1]

Copyright © 2015 by The American Association of Immunologists, Inc. Rhinovirus (RV) infections are common and have the potential to exacerbate asthma. We have determined the lung ... [more]

Copyright © 2015 by The American Association of Immunologists, Inc. Rhinovirus (RV) infections are common and have the potential to exacerbate asthma. We have determined the lung transcriptome in RV strain 1B-infected naive BALB/c mice (nonallergic) and identified CCL7 and IFN regulatory factor (IRF)-7 among the most upregulated mRNA transcripts in the lung. To investigate their roles we employed anti-CCL7 Abs and an IRF-7-targeting small interfering RNA in vivo. Neutralizing CCL7 or inhibiting IRF-7 limited neutrophil and macrophage influx and IFN responses in nonallergic mice. Neutralizing CCL7 also reduced activation of NF-¿B p65 and p50 subunits, as well as airway hyperreactivity (AHR) in nonallergic mice. However, neither NF-¿B subunit activation nor AHR was abolished with infection of allergic mice after neutralizing CCL7, despite a reduction in the number of neutrophils, macrophages, and eosinophils. IRF-7 small interfering RNA primarily suppressed IFN-a and IFN-b levels during infection of allergic mice. Our data highlight a pivotal role of CCL7 and IRF-7 in RV-induced inflammation and IFN responses and link NF-¿B signaling to the development of AHR.

DOI 10.4049/jimmunol.1401362
Citations Scopus - 23Web of Science - 24
Co-authors Paul Foster, Jason Girkin, Adam Collison, Nathan Bartlett
2015 Tay HL, Kaiko GE, Plank M, Li JJ, Maltby S, Essilfie AT, et al., 'Antagonism of miR-328 Increases the Antimicrobial Function of Macrophages and Neutrophils and Rapid Clearance of Non-typeable Haemophilus Influenzae (NTHi) from Infected Lung', PLoS Pathogens, 11 (2015) [C1]

© 2015 Tay et al. Pathogenic bacterial infections of the lung are life threatening and underpin chronic lung diseases. Current treatments are often ineffective potentially due to ... [more]

© 2015 Tay et al. Pathogenic bacterial infections of the lung are life threatening and underpin chronic lung diseases. Current treatments are often ineffective potentially due to increasing antibiotic resistance and impairment of innate immunity by disease processes and steroid therapy. Manipulation miRNA directly regulating anti-microbial machinery of the innate immune system may boost host defence responses. Here we demonstrate that miR-328 is a key element of the host response to pulmonary infection with non-typeable haemophilus influenzae and pharmacological inhibition in mouse and human macrophages augments phagocytosis, the production of reactive oxygen species, and microbicidal activity. Moreover, inhibition of miR-328 in respiratory models of infection, steroid-induced immunosuppression, and smoke-induced emphysema enhances bacterial clearance. Thus, miRNA pathways can be targeted in the lung to enhance host defence against a clinically relevant microbial infection and offer a potential new anti-microbial approach for the treatment of respiratory diseases.

DOI 10.1371/journal.ppat.1004549
Citations Scopus - 38Web of Science - 42
Co-authors Steven Maltby, Paul Foster, Philip Hansbro, Ming Yang, Gerard Kaiko, Hock Tay
2014 Starkey MR, Nguyen DH, Essilfie AT, Kim RY, Hatchwell LM, Collison AM, et al., 'Tumor necrosis factor-related apoptosis-inducing ligand translates neonatal respiratory infection into chronic lung disease.', Mucosal Immunol, 7 478-488 (2014) [C1]
DOI 10.1038/mi.2013.65
Citations Scopus - 31Web of Science - 31
Co-authors Paul Foster, Jay Horvat, Adam Collison, Philip Hansbro, Malcolm Starkey
2014 Mattes J, Gibson PG, 'The early origins of copd in severe asthma: The one thing that leads to another or the two things that come together?', Thorax, 69 789-790 (2014) [C3]
DOI 10.1136/thoraxjnl-2013-204815
Citations Scopus - 8Web of Science - 8
Co-authors Peter Gibson
2014 Mattes J, Murphy VE, Powell H, Gibson PG, 'Prenatal origins of bronchiolitis: Protective effect of optimised asthma management during pregnancy', Thorax, 69 383-384 (2014) [C1]

Objective Maternal asthma is the most common chronic disease complicating pregnancy and is a risk factor for bronchiolitis in infancy. Recurrent episodes of bronchiolitis are stro... [more]

Objective Maternal asthma is the most common chronic disease complicating pregnancy and is a risk factor for bronchiolitis in infancy. Recurrent episodes of bronchiolitis are strongly associated with the development of childhood asthma. Methods We conducted a follow-up study of infants born to women with asthma who completed a double-blind randomised controlled trial during pregnancy. In this trial, pregnant women with asthma were assigned to treatment adjustment by an algorithm using clinical symptoms (clinical group) or the fraction of exhaled nitric oxide (FeNO group) and we showed that the FeNO group had significantly lower asthma exacerbation rates in pregnancy. Results 146 infants attended the 12-month follow-up visit. Infants born to mothers from the FeNO group were significantly less likely to have recurrent episodes of bronchiolitis in the first year of life (OR 0.08, 95% CI 0.01 to 0.62; p=0.016) as compared with the clinical group. Conclusions Optimised management of asthma during pregnancy may reduce recurrent episodes of bronchiolitis in infancy, which could potentially modulate the risk to develop or the severity of emerging childhood asthma.

DOI 10.1136/thoraxjnl-2013-203388
Citations Scopus - 28Web of Science - 25
Co-authors Vanessa Murphy, Peter Gibson
2014 Hatchwell L, Girkin J, Morten M, Collison A, Mattes J, Foster PS, et al., 'Salmeterol attenuates chemotactic responses in rhinovirus-induced exacerbation of allergic airways disease by modulating protein phosphatase 2A', Journal of Allergy and Clinical Immunology, (2014) [C1]

Background: ß-Agonists are used for relief and control of asthma symptoms by reversing bronchoconstriction. They might also have anti-inflammatory properties, but the underpinning... [more]

Background: ß-Agonists are used for relief and control of asthma symptoms by reversing bronchoconstriction. They might also have anti-inflammatory properties, but the underpinning mechanisms remain poorly understood. Recently, a direct interaction between formoterol and protein phosphatase 2A (PP2A) has been described in¿vitro. Objective: We sought to elucidate the molecular mechanisms by which ß-agonists exert anti-inflammatory effects in allergen-driven and rhinovirus 1B-exacerbated allergic airways disease (AAD). Methods: Mice were sensitized and then challenged with house dust mite to induce AAD while receiving treatment with salmeterol, formoterol, or salbutamol. Mice were also infected with rhinovirus 1B to exacerbate lung inflammation and therapeutically administered salmeterol, dexamethasone, or the PP2A-activating drug (S)-2-amino-4-(4-[heptyloxy]phenyl)-2-methylbutan-1-ol (AAL[S]). Results: Systemic or intranasal administration of salmeterol protected against the development of allergen- and rhinovirus-induced airway hyperreactivity and decreased eosinophil recruitment to the lungs as effectively as dexamethasone. Formoterol and salbutamol also showed anti-inflammatory properties. Salmeterol, but not dexamethasone, increased PP2A activity, which reduced CCL11, CCL20, and CXCL2 expression and reduced levels of phosphorylated extracellular signal-regulated kinase 1 and active nuclear factor ¿B subunits in the lungs. The anti-inflammatory effect of salmeterol was blocked by targeting the catalytic subunit of PP2A with small RNA interference. Conversely, increasing PP2A activity with AAL(S) abolished rhinovirus-induced airway hyperreactivity, eosinophil influx, and CCL11, CCL20, and CXCL2 expression. Salmeterol also directly activated immunoprecipitated PP2A in¿vitro isolated from human airway epithelial cells. Conclusions: Salmeterol exerts anti-inflammatory effects by increasing PP2A activity in AAD and rhinovirus-induced lung inflammation, which might potentially account for some of its clinical benefits. © 2013 American Academy of Allergy, Asthma & Immunology.

DOI 10.1016/j.jaci.2013.11.014
Citations Scopus - 26Web of Science - 25
Co-authors Paul Foster, Nikki Verrills, Jason Girkin, Matt Dun, Adam Collison
2014 Tay HL, Plank M, Collison A, Mattes J, Kumar RK, Foster PS, 'MicroRNA: Potential biomarkers and therapeutic targets for allergic asthma?', Annals of Medicine, 46 633-639 (2014) [C1]

© 2014 Informa UK, Ltd. MicroRNAs are small non-coding RNAs that bind to multiple target mRNAs to control gene expression post-transcriptionally by inhibiting translation. In mamm... [more]

© 2014 Informa UK, Ltd. MicroRNAs are small non-coding RNAs that bind to multiple target mRNAs to control gene expression post-transcriptionally by inhibiting translation. In mammalian cells, microRNAs play important roles in a diverse array of cellular processes (e.g. cell proliferation and differentiation). However, alterations in their levels may compromise cellular function, predisposing to disease. In this review, we discuss microRNAs that have been linked with pathogenesis of asthma and propose functional roles in the regulation of disease. MicroRNAs have the potential to be biomarkers for asthma and provide the platform for the development of new classes of therapeutic compounds.

DOI 10.3109/07853890.2014.958196
Citations Scopus - 19Web of Science - 17
Co-authors Adam Collison, Hock Tay, Paul Foster
2014 Murphy VE, Mattes J, Powell H, Baines KJ, Gibson PG, 'Respiratory viral infections in pregnant women with asthma are associated with wheezing in the first 12 months of life', Pediatric Allergy and Immunology, 25 151-158 (2014) [C1]

Background: There are few studies investigating the relationship between respiratory viral infection in pregnancy and asthma in the offspring, and none among mothers with asthma. ... [more]

Background: There are few studies investigating the relationship between respiratory viral infection in pregnancy and asthma in the offspring, and none among mothers with asthma. Infants of mothers with asthma are more likely to wheeze and have a higher risk of developing asthma than infants of non-asthmatic mothers. Methods: A prospective cohort study of viral infection in pregnancy was conducted between 2007 and 2009, and a subgroup of infants of mothers with asthma was followed up at 6 and 12 months of age. During common colds, nasal and throat swabs were collected from mothers and respiratory viruses detected by polymerase chain reaction. Respiratory health of infants was assessed by parent-completed questionnaire. Results: Twelve-month-old infants whose mothers had confirmed viral infections in pregnancy (n = 26) reported more frequent wheeze (40% had 4-12 wheeze attacks compared with 0%), sleep disturbed by wheeze (1 night per week or more in 60% vs. 11%), beta agonist treatment for wheeze (27% vs. 0%), prolonged colds (2 wk or longer 31% vs. 0%), more eczema (40% vs. 6.3%), and parent-perceived asthma (32% vs. 0%), compared with infants whose mothers had common colds without laboratory-confirmed viral infection (n = 16). Conclusions: This study demonstrates a relationship between maternal respiratory viral infection in pregnancy and wheezing illness in infants of mothers with asthma. Viral infections are the most common cause of asthma exacerbations in pregnancy, and infants of asthmatic mothers are at increased risk of asthma themselves. Further research is needed to elucidate the mechanisms involved. © 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

DOI 10.1111/pai.12156
Citations Scopus - 12Web of Science - 12
Co-authors Katherine Baines, Peter Gibson, Vanessa Murphy
2014 Preece K, Bhatia R, Belcher J, Patchett K, McElduff P, Collison A, Mattes J, 'The fraction of exhaled nitric oxide improves prediction of clinical allergic reaction to peanut challenge in children', CLINICAL AND EXPERIMENTAL ALLERGY, 44 371-380 (2014) [C1]
DOI 10.1111/cea.12258
Citations Scopus - 4Web of Science - 5
Co-authors Adam Collison, Patrick Mcelduff
2014 Pinnock R, Monagle P, Couper J, Wright I, Asher I, Jones P, et al., 'Dedicated paediatric teaching remains critical to the undergraduate medical curriculum', JOURNAL OF PAEDIATRICS AND CHILD HEALTH, 50 949-951 (2014) [C3]
DOI 10.1111/jpc.12775
Co-authors Ian Wright
2014 Wark PAB, Murphy V, Mattes J, 'The interaction between mother and fetus and the development of allergic asthma', Expert Review of Respiratory Medicine, 8 57-66 (2014) [C1]

The rising prevalence of asthma and atopic disease in industrialized countries in the last 50 years has raised important questions about how and why the disease develops in suscep... [more]

The rising prevalence of asthma and atopic disease in industrialized countries in the last 50 years has raised important questions about how and why the disease develops in susceptible populations. Most asthma begins in childhood in association with allergic sensitization and the development of a TH2 phenotype. It is recognized that asthma arises in the context of a complex interaction between genetic factors and the evolving immune system of the infant and the environment to which it is exposed, which now includes its in utero exposure. Early life exposures that lead to allergen sensitization and airway damage, especially in the form of viral respiratory tract infections, may lead to disease induction that commence the process that leads in some to asthma. Asthma models and early life observations suggest that repeated exposure to allergens and viral infection perpetuate a state of chronic airway inflammation leading to a maladaptive innate immune response that fails to resolve, characterized by chronic airway inflammation, airway remodeling and airway hyperresponsiveness. This article will concentrate on the development of asthma in the context of early life and maternal influences, including the effect of asthma on both the fetus and the mother. © 2014 Informa UK Ltd.

DOI 10.1586/17476348.2014.848795
Citations Scopus - 10Web of Science - 11
Co-authors Peter Wark, Vanessa Murphy
2014 Hansbro PM, Starkey MR, Mattes J, Horvat JC, 'Pulmonary immunity during respiratory infections in early life and the development of severe asthma', Annals of the American Thoracic Society, 11 S297-S302 (2014) [C1]

Copyright © 2014 by the American Thoracic Society Asthma affects 10% of the population in Westernized countries, being most common in children. It is a heterogeneous condition cha... [more]

Copyright © 2014 by the American Thoracic Society Asthma affects 10% of the population in Westernized countries, being most common in children. It is a heterogeneous condition characterized by chronic allergic airway inflammation, mucus hypersecretion, and airway hyperresponsiveness (AHR) to normally innocuous antigens. Combination therapies with inhaled corticosteroids and bronchodilators effectively manage mild to moderate asthma, but there are no cures, and patients with severe asthma do not respond to these treatments. The inception of asthma is linked to respiratory viral (respiratory syncytial virus, rhinovirus) and bacterial (Chlamydia, Mycoplasma) infections. The examination of mouse models of early-life infections and allergic airway disease (AAD) provides valuable insights into the mechanisms of disease inception that may lead to the development of more effective therapeutics. For example, early-life, but not adult, Chlamydia respiratory infections in mice permanently modify immunity and lung physiology. This increases the severity of AAD by promoting IL-13 expression, mucus hypersecretion, and AHR. We have identified novel roles for tumor necrosis factor-related apoptosisinducing ligand (TRAIL) and IL-13 in promoting infection-induced pathology in early life and subsequent chronic lung disease. Genetic deletion of TRAIL or IL-13 variously protected against neonatal infection-induced inflammation, mucus hypersecretion, altered lung structure, AHR, and impaired lung function. Therapeutic neutralization of these factors prevented infection-induced severe AAD. Other novel mechanisms and avenues for intervention are also being explored. Such studies indicate the immunological mechanisms that may underpin the association between early-life respiratory infections and the development of more severe asthma and may facilitate the development of tailored preventions and treatments.

DOI 10.1513/AnnalsATS.201402-086AW
Citations Scopus - 22
Co-authors Jay Horvat, Malcolm Starkey, Philip Hansbro
2014 Gunawardhana LP, Baines KJ, Mattes J, Murphy VE, Simpson JL, Gibson PG, 'Differential DNA methylation profiles of infants exposed to maternal asthma during pregnancy', Pediatric Pulmonology, 49 852-862 (2014) [C1]

Background Asthma is a complex disease that involves both genetic factors and environmental exposures. Aberrant epigenetic modifications, such as DNA methylation, may be important... [more]

Background Asthma is a complex disease that involves both genetic factors and environmental exposures. Aberrant epigenetic modifications, such as DNA methylation, may be important in asthma development. Fetal exposure to maternal asthma during critical periods of in utero development may lead to epigenetic alterations that predispose infants to a greater risk of developing asthma themselves. We investigated alterations in the DNA methylation profile of peripheral blood from infants exposed to maternal asthma during pregnancy. Methods Peripheral blood was collected from 12-month-old infants born to women with (n = 25) and without (n = 15) doctor diagnosed asthma during pregnancy. Genomic DNA was extracted, bisulfite converted, and hybridized to Infinium Methylation 27 arrays (Illumina), containing over27,000 CpGs from 14,495 genes. CpG loci in only autosomal genes were classified as differentially methylated at the 99% level (P < 0.01, |DiffScore| > 22 and delta beta >0.06). Results There were 70 CpG loci, corresponding to 67 genes that were significantly differentially methylated. Twelve CpG loci (11 genes) showed greater than 10% comparative difference in DNA methylation, including hyper-methylated loci of FAM181A, MRI1, PIWIL1, CHFR, DEFA1, MRPL28, AURKA, and hypo-methylated loci of NALP1L5, MAP8KIP3, ACAT2, and PM20D1 in maternal asthma. Methylation of MAPK8IP3 was significantly negatively correlated with maternal blood eosinophils (r = -0.38; P = 0.022), maternal eNO (r = -0.44; P = 0.005), and maternal serum total IgE (r = -0.39, P = 0.015). Methylation of AURKA negatively correlated with maternal hemoglobin (r = -0.43; P = 0.008), infants height (r = -0.51; P < 0.001) and weight (r = -0.36; P = 0.021). Methylation of PM20D1 was lower in infants born to mothers with asthma on inhaled corticosteroid treatment. Methylation of PM20D1 was lower and MRI1 was higher in infants born to atopic mothers without asthma. Conclusions In an Australian study population, exposure to maternal asthma during pregnancy is associated with differential methylation profiles of infants' peripheral blood DNA, which may act as risk factors for future asthma development. © 2013 Wiley Periodicals, Inc.

DOI 10.1002/ppul.22930
Citations Scopus - 31Web of Science - 28
Co-authors Peter Gibson, Katherine Baines, Vanessa Murphy, Jodie Simpson
2014 Collison A, Li J, Pereira De Siqueira A, Zhang J, Toop HD, Morris JC, et al., 'Tumor necrosis factor-related apoptosis-inducing ligand regulates hallmark features of airways remodeling in allergic airways disease', American Journal of Respiratory Cell and Molecular Biology, 51 86-93 (2014) [C1]

Allergic asthma is a complex disease characterized by acute inflammation of the airways that over time leads to the development of significant structural changes termed remodeling... [more]

Allergic asthma is a complex disease characterized by acute inflammation of the airways that over time leads to the development of significant structural changes termed remodeling. TNF-related apoptosis-inducing ligand (TRAIL) has an important regulatory role in acute allergic airways inflammation through up-regulation of the E3 ubiquitin ligase Midline-1 (MID-1), which limits protein phosphatase 2A (PP2A) activity and downstream dephosphorylation of proinflammatory signaling molecules. The relevance of TRAIL in the development of airways remodeling has yet to be determined. In this study, the lungs of wild-type (WT) BALB/c and Tnfsf10 knockout (TRAIL-/-) mice were chronically exposed to ovalbumin (OVA) for 12 weeks to induce hallmark features of chronic allergic airways disease, including airways hyperreactivity (AHR), subepithelial collagen deposition, goblet cell hyperplasia, and smooth muscle hypertrophy. TRAIL-/- mice were largely protected from the development of AHR and peribronchial eosinophilia and had reduced levels of mast cells in the airways. This correlated with lower levels of cytokines, including IL-4, -5, -10, and -13, and with lower levels of proinflammatory chemokines from cultured cells isolated from the draining lymph nodes. TRAIL-/- mice were also protected from the characteristic features of airways remodeling, including peribronchial fibrosis, smooth muscle hypertrophy, and mucus hypersecretion, which correlated with reduced TGF-ß1 levels in the lungs. MID-1 expression was reduced in TRAIL-/- mice and up-regulated in allergic WT mice. Raising PP2A activity using 2-amino-4-(4-heptyloyphenol)-2-methylbutan-1-ol in allergic WT mice reduced eosinophilia, TGF-ß1, and peribronchial fibrosis. This study shows that TRAIL promotes airways remodeling in an OVA-induced model of chronic allergic airways disease. Targeting TRAIL and its downstream proin flammatory signaling pathway involving PP2A may be of therapeutic bene fit in reducing the hallmark features of airways remodeling observed in chronic allergic airways inflammation. Copyright © 2014 by the American Thoracic Society.

DOI 10.1165/rcmb.2013-0490OC
Citations Scopus - 26Web of Science - 24
Co-authors Adam Collison, Paul Foster
2013 de Souza Alves CC, Collison A, Hatchwell L, Plank M, Morten M, Foster PS, et al., 'Inhibiting AKT phosphorylation employing non-cytotoxic anthraquinones ameliorates TH2 mediated allergic airways disease and rhinovirus exacerbation.', PLoS One, 8 e79565 (2013) [C1]
DOI 10.1371/journal.pone.0079565
Citations Scopus - 17Web of Science - 15
Co-authors Adam Collison, Paul Foster
2013 Foster PS, Plank MW, Collison AM, Tay HL, Kaiko GE, Li J, et al., 'The emerging role of microRNAs in regulating immune and inflammatory responses in the lung', Immunological Reviews, 253 198-215 (2013) [C1]
Citations Scopus - 66Web of Science - 68
Co-authors Ming Yang, Philip Hansbro, Hock Tay, Paul Foster, Gerard Kaiko, Adam Collison
2013 Plank M, Maltby S, Mattes J, Foster PS, 'Targeting translational control as a novel way to treat inflammatory disease: The emerging role of MicroRNAs', Clinical and Experimental Allergy, 43 981-999 (2013) [C1]

Chronic inflammatory diseases (e.g. asthma and chronic obstructive pulmonary disease) are leading causes of morbidity and mortality world-wide and effective treatments are limited... [more]

Chronic inflammatory diseases (e.g. asthma and chronic obstructive pulmonary disease) are leading causes of morbidity and mortality world-wide and effective treatments are limited. These disorders can often be attributed to abnormal immune responses to environmental stimuli and infections. Mechanisms leading to inflammation are complex, resulting from interactions of structural cells and activation of both the adaptive and innate arms of the immune system. The activation of structural and immune cells involves both temporary and permanent changes in gene expression in these cells, which underpin chronic inflammation and tissue dysfunction. miRNAs are small non-coding RNAs increasingly being recognized to play important roles in the post-transcriptional regulation of gene expression in mammalian cells by regulating translation. Individual miRNAs can exert their effects by directly inhibiting the translation or stability of multiple mRNAs simultaneously. Thus, the expression or blockade of function of a single miRNA (miR) can result in pronounced alterations in protein expression within a given cell. Dysregulation of miRNA expression may subsequently alter cellular function, and in certain situations predispose to disease. Our current understanding of the role of miRNA in the regulation of inflammatory disease (e.g. allergic diseases) remains limited. In this review, we provide an overview of the current understanding of miRNA biogenesis and function, the roles miRNA play in the regulation of immune cell function and their potential contribution to inflammatory diseases. We also highlight strategies to alter miRNA function for experimental or therapeutic gain, and discuss the potential utility and limitations of targeting these molecules as anti-inflammatory strategies. © 2013 John Wiley & Sons Ltd.

DOI 10.1111/cea.12135
Citations Scopus - 39Web of Science - 41
Co-authors Paul Foster, Steven Maltby
2013 Plank M, Maltby S, Mattes J, Foster PS, 'Targeting translational control as a novel way to treat inflammatory disease: the emerging role of microRNAs.', Clinical and Experimental Allergy, 43 981-999 (2013)
DOI 10.1111/cea.12170
Co-authors Paul Foster, Steven Maltby
2013 Barry J, Loh Z, Collison A, Mazzone S, Lalwani A, Zhang V, et al., 'Absence of Toll-IL-1 Receptor 8/Single Immunoglobulin IL-1 Receptor-Related Molecule Reduces House Dust Mite-Induced Allergic Airway Inflammation in Mice', AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 49 481-490 (2013) [C1]
DOI 10.1165/rcmb.2012-0425OC
Citations Scopus - 15Web of Science - 16
Co-authors Paul Foster, Adam Collison
2013 Collison AM, Hatchwell LM, Verrills NM, Wark PA, Pereira De Siqueira AL, Tooze MK, et al., 'The E3 ubiquitin ligase midline 1 promotes allergen and rhinovirus-induced asthma by inhibiting protein phosphatase 2A activity', Nature Medicine, 19 232-237 (2013) [C1]
Citations Scopus - 90Web of Science - 88
Co-authors Peter Wark, Nikki Verrills, Adam Collison, Nathan Bartlett, Paul Foster
2013 Collison A, Siegle JS, Hansbro NG, Kwok C-T, Herbert C, Mattes J, et al., 'Epigenetic changes associated with disease progression in a mouse model of childhood allergic asthma', DISEASE MODELS & MECHANISMS, 6 993-1000 (2013) [C1]
DOI 10.1242/dmm.011247
Citations Scopus - 14Web of Science - 13
Co-authors Nicole Hansbro, Paul Foster, Adam Collison
2013 Starkey MR, Essilfie A-T, Horvat JC, Kim RY, Nguyen DH, Beagley KW, et al., 'Constitutive production of IL-13 promotes early-life Chlamydia respiratory infection and allergic airway disease', Mucosal Immunology, 6 569-579 (2013) [C1]
Citations Scopus - 36Web of Science - 36
Co-authors Malcolm Starkey, Philip Hansbro, Paul Foster, Jay Horvat
2012 Starkey MR, Kim RY, Beckett EL, Schilter HC, Shim D, Essilfie A-T, et al., 'Chlamydia muridarum lung infection in infants alters hematopoietic cells to promote allergic airway disease in mice', PLoS One, 7 (2012) [C1]
DOI 10.1371/journal.pone.0042588
Citations Scopus - 22Web of Science - 23
Co-authors Philip Hansbro, Jay Horvat, Malcolm Starkey, Emma Beckett
2011 Collison AM, Herbert C, Siegle JS, Mattes J, Foster PS, Kumar RK, 'Altered expression of microRNA in the airway wall in chronic asthma: miR-126 as a potential therapeutic target', BMC Pulmonary Medicine, 11 29 (2011) [C1]
Citations Scopus - 99Web of Science - 95
Co-authors Adam Collison, Paul Foster
2011 Collison AM, Mattes J, Plank MW, Foster PS, 'Inhibition of house dust mite-induced allergic airways disease by antagonism of microRNA-145 is comparable to glucocorticoid treatment', Journal of Allergy and Clinical Immunology, 128 160-U251 (2011) [C1]
Citations Scopus - 154Web of Science - 143
Co-authors Adam Collison, Paul Foster
2011 Weckmann M, Kopp MV, Heinzmann A, Mattes J, 'Haplotypes covering the TNFSF10 gene are associated with bronchial asthma', Pediatric Allergy and Immunology, 22 25-30 (2011) [C1]
DOI 10.1111/j.1399-3038.2010.01027.x
Citations Scopus - 5Web of Science - 5
2009 Tran HA, Song S, Crock PA, Mattes J, Howard K, 'The A, B, C, D of hypercalcaemia in Down syndrome', BMJ Case Reports, (2009) [C1]

Hypercalcaemia in infants with Down syndrome is an uncommon condition with only five previous case reports. The patients often present in the toddler years with the classical tria... [more]

Hypercalcaemia in infants with Down syndrome is an uncommon condition with only five previous case reports. The patients often present in the toddler years with the classical triad of Down syndrome, biochemical hypercalcaemia, and nephrocalcinosis. We present the sixth case and second male with this condition and further review the clinical details of this under-recognised condition and stratify the diagnostic criteria. The management mandates a reduction in calcium intake as a first step. The natural history of the various aspects of this condition is also considered.

DOI 10.1136/bcr.06.2008.0232
Citations Scopus - 4
2009 Mattes J, Collison AM, Plank MW, Phipps S, Foster PS, 'Antagonism of microRNA-126 suppresses the effector function of T(H)2 cells and the development of allergic airways disease', Proceedings of the National Academy of Sciences of the United States of America, 106 18704-18709 (2009) [C1]
DOI 10.1073/pnas.0905063106
Citations Scopus - 311Web of Science - 297
Co-authors Adam Collison, Paul Foster
2009 Collison AM, Foster PS, Mattes J, 'Emerging role of tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) as a key regulator of inflammatory responses', Clinical and Experimental Pharmacology and Physiology, 36 1049-1053 (2009) [C1]
DOI 10.1111/j.1440-1681.2009.05258.x
Citations Scopus - 43Web of Science - 43
Co-authors Paul Foster, Adam Collison
2009 Foster PS, Mattes J, 'IL-21 comes of age', Immunology and Cell Biology, 87 359-360 (2009) [C2]
DOI 10.1038/icb.2009.33
Citations Scopus - 3Web of Science - 3
Co-authors Paul Foster
2009 Phipps S, Lam CE, Kaiko GE, Foo A, Collison AM, Mattes J, et al., 'Toll/IL-1 signaling is critical for house dust mite-specific Th1 and Th2 responses', American Journal of Respiratory and Critical Care Medicine, 179 883-893 (2009) [C1]
DOI 10.1164/rccm.200806-974oc
Citations Scopus - 127Web of Science - 125
Co-authors Gerard Kaiko, Adam Collison, Paul Foster
2008 Mattes J, Collison AM, Foster PS, 'Emerging role of microRNAs in disease pathogenesis and strategies for therapeutic modulation', Current Opinion in Molecular Therapeutics, 10 150-157 (2008) [C1]
Citations Scopus - 49Web of Science - 47
Co-authors Paul Foster, Adam Collison
2008 Yang M, Mattes J, 'Discovery, biology and therapeutic potential of RNA interference, microRNA and antagomirs', Pharmacology & Therapeutics, 117 94-104 (2008) [C1]
DOI 10.1016/j.pharmthera.2007.08.004
Citations Scopus - 75Web of Science - 70
Co-authors Ming Yang
2007 Mattes J, Yang M, Foster PS, 'Regulation of microRNA by antagomirs: a new class of pharmacological antagonists for the specific regulation of gene function?', American Journal of Respiratory and Cellular Molecular Biology, 36 8-12 (2007) [C1]
DOI 10.1165/rcmb.2006-0227TR
Citations Scopus - 60Web of Science - 55
Co-authors Paul Foster, Ming Yang
2007 Weckmann M, Collison A, Simpson JL, Kopp MV, Wark PA, Smyth MJ, et al., 'Critical link between TRAIL and CCL20 for the activation of T(H)2 cells and the expression of allergic airway disease', Nature Medicine, 13 1308-1315 (2007) [C1]
DOI 10.1038/nm1660
Citations Scopus - 92Web of Science - 90
Co-authors Jodie Simpson, Paul Foster, Peter Gibson, Peter Wark, Adam Collison, Nicole Hansbro
2007 Huck B, Neumann-Haefelin D, Schmitt-Graeff A, Weckmann M, Mattes J, Ehl S, Falcone V, 'Human metapneumovirus induces more severe disease and stronger innate immune response in BALB/c mice as compared with respiratory syncytial virus', Respiratory Research, 8 (2007) [C1]
DOI 10.1186/1465-9921-8-6
Citations Scopus - 34Web of Science - 33
2007 Mattes J, Whitehead BF, Liehr T, Wilkinson I, Bear J, Fagan KA, et al., 'Paternal uniparental isodisomy for chromosome 14 with mosaicism for a supernumerary marker chromosome 14', American Journal of Medical Genetics Part A, 143A 2165-2171 (2007) [C1]
DOI 10.1002/ajmg.a.31896
Citations Scopus - 17Web of Science - 16
2006 Yang M, Mattes J, Hansbro PM, Foster PS, 'Employment of microRNA profiles and RNA interference and antagomirs for the characterization and treatment of respiratory disease', Drug Discovery Today: Therapeutic Strategies, 3 325-332 (2006) [C1]
DOI 10.1016/j.ddstr.2006.10.001
Citations Scopus - 5
Co-authors Philip Hansbro, Ming Yang, Paul Foster
2005 Prescott VE, Campbell PM, Moore A, Mattes J, Rothenberg ME, Foster PS, et al., 'Transgenic expression of bean alpha-amylase inhibitor in peas results in altered structure and immunogenicity', Journal of Agricultural and Food Chemistry, 53 9023-9030 (2005) [C1]
DOI 10.1021/jf050594v
Citations Scopus - 140Web of Science - 112
Co-authors Paul Foster
2004 Clark K, Simson L, Newcombe N, Koskinen AML, Mattes J, Lee NA, et al., 'Eosinophil degranulation in the allergic lung of mice primarily occurs in the airway lumen', Journal of Leukocyte Biology, 75 1001-1009 (2004) [C1]
DOI 10.1189/jlb.0803391
Citations Scopus - 44Web of Science - 41
Co-authors Paul Foster
2004 Ihorst G, Frischer T, Horak F, Schumacher M, Kopp M, Forster J, et al., 'Long- and medium-term ozone effects on lung growth including a broad spectrum of exposure', EUROPEAN RESPIRATORY JOURNAL, 23 292-299 (2004)
DOI 10.1183/09031936.04.00021704
Citations Scopus - 30Web of Science - 26
2004 Storm Van's Gravesande K, Mattes J, Endlicher A, Alving K, Ihorst G, Kühr J, 'Effect of two doses of budesonide on exhaled nitric oxide and urinary EPX excretion in asthmatic children', Pneumologie, 58 483-488 (2004)

The use of objective outcome measures that assess airway inflammation in pediatric asthma can provide a good evaluation of asthma severity and treatment response. In this double-b... [more]

The use of objective outcome measures that assess airway inflammation in pediatric asthma can provide a good evaluation of asthma severity and treatment response. In this double-blind and randomized study the effects of 200 µg of budesonide and 800 µg of budesonide on markers of inflammation (exhaled nitric oxide (eNO), eosinophil protein X (EPX) excretion in urine) and on lung function (FEV 1) were prospectively investigated in 24 ICS-naive children with mild persistent to moderate persistent asthma over a period of eight weeks. After eight weeks of treatment 200 µg and 800 µg of budesonide led to a significant decrease (p < 0.025) in eNO [median (90% interval): 200 µg: -17.2 ppb (-54.6 to 0.9); 800 µg: -13.2 ppb (-44.6 to -1.7)]. A significant change in urinary EPX excretion was only observed in the high dose group [200 µg: -10.3 µg/mmol creatinine (-116.2 to 50.5), p = 0.9; 800 µg: -49.2 µg/mmol creatinine (-231.0 to 48.7), p = 0.02]. However, a significant difference between the change from baseline after 8 weeks of either group was found neither for eNO (p = 0.66) nor for EPX excretion (p = 0.04). In conclusion, our data demonstrate that 800 µg budesonide per day did not show any advantage in reduction of airway inflammation, measured by eNO and urinary EPX excretion, in children with mild persistent to moderate persistent asthma.

DOI 10.1055/s-2004-818466
Citations Scopus - 3
2004 Ngoumou G, Schaefer DO, Mattes J, Kopp MV, 'Interleukin-18 enhances the production of interferon-gamma (IFN-gamma) by allergen-specific and unspecific stimulated cord blood mononuclear cells', CYTOKINE, 25 172-178 (2004)
DOI 10.1016/j.cyto.2003.11.013
Citations Scopus - 4Web of Science - 5
2003 Mattes J, Foster P, 'Regulation of eosinophil migration and Th2 cell function by IL-5 and eotaxin', Current Drug Targets, 2 169-174 (2003) [C1]
Citations Scopus - 44
Co-authors Paul Foster
2003 Foster PS, Yang M, Mattes J, Kumar R, Webb D, 'Interleukin-13 and allergy', Modern Aspects of Immunobiology, 3 8 (2003)
Co-authors Ming Yang, Paul Foster
2003 Mattes J, Hulett M, Xie W, Hogan S, Rothenburg ME, Foster P, Parish C, 'Immunotherapy of cytotoxic T cell resistant tumors by T helper 2 cells: an eotaxin and STAT6 dependent process', Journal of Experimental Medicine, 197 387-393 (2003) [C1]
DOI 10.1084/jem.20021683
Citations Scopus - 160Web of Science - 149
Co-authors Paul Foster
2003 Kruse S, Kuehr J, Moseler M, Kropp MV, Kurz T, Deichmann KA, et al., 'Polymorphisms in the IL18 gene are associated with specific sensitization to common allergens and allergic rhinitis', Journal of Allergy and Clinical Immunology, 111 117-122 (2003) [C1]
DOI 10.1067/mai.2003.43
Citations Scopus - 117Web of Science - 101
Co-authors Paul Foster
2003 Lange J, Ngoumou G, Berkenheide S, Moseler M, Mattes J, Kuehr J, Kopp MV, 'High interleukin-13 production by phytohaemagglutinin- and Der p 1-stimulated cord blood mononuclear cells is associated with the subsequent development of atopic dermatitis at the age of 3 years', CLINICAL AND EXPERIMENTAL ALLERGY, 33 1537-1543 (2003)
DOI 10.1046/j.1365-2222.2003.01789.x
Citations Scopus - 30Web of Science - 25
2002 Mattes J, Yang M, Mahalinggam S, Kuehr J, Webb DC, Simson L, et al., 'Intrinsic defect in T cell production of interleukin (IL)-13 in the absence of both IL-5 and cotaxin precludes the development of eosinophilia and airways hyperreactivity in experimental asthma.', J Exp Med. 195:1433-44, 1433-1444 (2002) [C1]
Citations Scopus - 216Web of Science - 203
Co-authors Ming Yang, Paul Foster
2002 Mattes J, Gravesande KSV, Moeller C, Moseler M, Brandis M, Kuehr J, 'Circadian variation of exhaled nitric oxide and urinary eosinophil protein X in asthmatic and healthy children', PEDIATRIC RESEARCH, 51 190-194 (2002)
DOI 10.1203/00006450-200202000-00011
Citations Scopus - 35Web of Science - 33
2002 Foster PS, Hogan S, Yang M, Mattes J, Young I, Matthaei K, et al., 'Interleukin-5 and eosinophils as therapeutic targets for asthma', Trends in Molecular Medicine, 8 162-167 (2002) [C2]
Citations Scopus - 63Web of Science - 57
Co-authors Ming Yang, Paul Foster
2002 Karmaus W, Arshad H, Mattes J, 'Re: "Does the sibling effect have its origin in utero? Investigating birth order, cord blood immunoglobulin E concentration, and allergic sensitization at age 4 years" - Reply', AMERICAN JOURNAL OF EPIDEMIOLOGY, 156 883-884 (2002)
DOI 10.1093/aje/kwf123
2001 Karmaus W, Arshad H, Mattes J, 'Does the sibling effect have its origin in utero? Investigating birth order, cord blood immunoglobulin E concentration, and allergic sensitization at age 4 years', AMERICAN JOURNAL OF EPIDEMIOLOGY, 154 909-915 (2001)
DOI 10.1093/aje/154.10.909
Citations Scopus - 106Web of Science - 108
2001 Hertz M, Mahalingam S, Dalum I, Klysner S, Mattes J, Neisig A, et al., 'Active vaccination against IL-5 bypasses immunological tolerance and ameliorates experimental asthma', Journal of Immunology, 167 3792-3799 (2001) [C1]
Citations Scopus - 75Web of Science - 70
Co-authors Paul Foster
2001 Mackenzie J, Mattes J, Dent L, Foster PS, 'Eosinophils promote allergic disease of the lung by regulating CD4+ Th2 lymphocyte function', Journal of Immunology, 167 3146-3155 (2001) [C1]
Citations Scopus - 169Web of Science - 158
Co-authors Paul Foster
2001 Mattes J, Yang M, Siqueira A, Clark K, Mackenzie J, McKenzie A, et al., 'IL-13 induces airways hyperreactivity independently of the IL-4R{alpha} chain in the allergic lung', Journal of Immunology, 167 1683-1692 (2001) [C1]
Citations Scopus - 129Web of Science - 119
Co-authors Ming Yang, Paul Foster
2001 Foster PS, Mould A, Yang M, Mackenzie J, Mattes J, Hogan S, et al., 'Elemental signals regulating eosinophil accumulation in the lung', Immunological Reviews, 179 173-181 (2001) [C2]
Citations Scopus - 194Web of Science - 172
Co-authors Paul Foster, Ming Yang
2000 Webb D, McKenzie A, Koskinen A, Yang M, Mattes J, Foster PS, 'Integrated signals between IL-13, IL-4, and IL-5 regulate airways hyperreactivity', Journal of Immunology, 165 108-113 (2000) [C1]
Citations Scopus - 268Web of Science - 243
Co-authors Ming Yang, Paul Foster
2000 Mattes J, van's Gravesande KS, Moeller C, Kuehr J, 'Circadian variation of urinary EPX in asthmatic and healthy children', JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 105 S193-S193 (2000)
DOI 10.1016/S0091-6749(00)91008-X
2000 van Gravesande KS, Mattes J, Grossklauss E, Zurmuhl A, Moseler M, Kuhr J, 'Preventive effect of 2 and 10 mg of sodium cromoglycate on exercise-induced bronchoconstriction', EUROPEAN JOURNAL OF PEDIATRICS, 159 759-763 (2000)
DOI 10.1007/PL00008341
Citations Scopus - 8Web of Science - 3
2000 Reining U, Mattes J, Storm Van's Gravesande K, Ihorst G, Kühr J, 'Reproducibility in the induced sputum in childhood', Pneumologie, 54 185-190 (2000)

In asthmatic children sputum-induction with hypertonic saline is useful to quantify the eosinophilic inflammation. However, only few data are available about feasibility and safet... [more]

In asthmatic children sputum-induction with hypertonic saline is useful to quantify the eosinophilic inflammation. However, only few data are available about feasibility and safety of the procedure in children. Therefore, taking 9 non-atopic healthy control children (mean age 11,8 years) and 34 asthmatic children (mean age 11,4 years), inhaling n = 25 Budesonid (400-1200 µg/die) and n = 9 DNCG (60 mg/die), sputum induction was performed twice within 6 weeks. Briefly, 10 minutes after inhalation of 200 µg salbutamol subjects inhaled hypertonic saline (3, 4 and 5%) for in all 30 minutes, while all 5 minutes lung function was checked and expectoration of sputum was supported. Adequate sputum plugs were separated from contaminating saliva and processed immediately employing native chamber and cytospin cell count as well as measurement of eosinophilic: cationic protein (ECP). Sputum-induction could be performed in 84 out of 86 planed tests (97,7%) without any objective clinical adverse effects. The mean fall in FEV1 was 3,0%, the maximum 11,0%. The reproducibility of eosinophil, neutrophil and lymphocyte differential cell count (5-95%-values Test1: 0,0- 4.2%, 0,8 - 11,4%, and 3.2 - 35,1%, respectively) was moderate for eosinophils and neutrophils (Intraclass-Correlation-Coefficient (ICC) 0,41) as well as for lymphocytes (ICC = 0,49). For ECP 5-95%-values Test1: 39,8-8000.0 µg/l) only a fair reproducibility (ICC = 0,24) was found. The ICC levels for total cell count (ICC = 0,31) and for weight of the sputum plug (ICC = 0,30) were also fair. Based on the procedure presented induced sputum is a feasible and safe method in childhood. The differential sputum cell count of eosinophils, neutrophils and lymphocytes can be recommended as parameters with moderate reproducibility.

DOI 10.1055/s-2000-3828
Citations Scopus - 1
1999 Mattes J, Gravesande KS, Reining U, Alving K, Ihorst G, Henschen M, Kuehr J, 'NO in exhaled air is correlated with markers of eosinophilic airway inflammation in corticosteroid-dependent childhood asthma', EUROPEAN RESPIRATORY JOURNAL, 13 1391-1395 (1999)
DOI 10.1183/09031936.99.13613969
Citations Scopus - 130Web of Science - 113
1999 Mattes J, Karmaus W, 'The use of antibiotics in the first year of life and development of asthma: which comes first?', CLINICAL AND EXPERIMENTAL ALLERGY, 29 729-732 (1999)
Citations Scopus - 26Web of Science - 21
1999 van's Gravesande KS, Mattes J, Gruntjens T, Kopp M, Seydewitz HH, Moseler M, Kuehr J, 'Circadian variation of urinary eosinophil protein X in asthmatic and healthy children', CLINICAL AND EXPERIMENTAL ALLERGY, 29 1497-1501 (1999)
Citations Scopus - 18Web of Science - 14
1999 Bohnet W, Bar G, Strauch E, Ihorst G, Mattes J, Schneider C, et al., 'Short-term effect of particular matter (PM10) on pulmonary function in schoolchildren over two years', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 159 A772-A772 (1999)
1999 Mattes J, Baer G, Schneider C, Bohnet W, Ihorst G, Strauch E, et al., 'Association between respiratory symptoms and ambient ozone levels over two summers in 765 schoolchildren', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 159 A772-A772 (1999)
1999 Mattes J, Baer G, Schneider C, Bohnet W, Ihorst G, Strauch E, et al., 'Correlation between personal and fixed-site ozone measurements in schoolchildren', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 159 A772-A772 (1999)
1999 Mattes J, van Gravesande KS, Reining U, Alving K, Ihorst G, Heuschen M, Kuehr J, 'Nitric oxide in exhaled air is correlated with eosinophilic airway inflammation in children with chronic asthma', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 159 A862-A862 (1999)
1999 Gravesande KSV, Langenbacher E, Mattes J, Zurmuehl A, Beck W, Moseler M, Knehr J, 'Sodium cromoglycate (SCG) reduces the excretion of eosinophil protein X (EPX) in children with exercise induced asthma', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 159 A911-A911 (1999)
1999 Mattes J, Karmaus W, Gravesande KSV, Moseler M, Forster J, Kuehr J, 'Pulmonary function in children of school age is related to the number of siblings in their family', PEDIATRIC PULMONOLOGY, 28 414-417 (1999)
DOI 10.1002/(SICI)1099-0496(199912)28:6&lt;414::AID-PPUL5&gt;3.0.CO;2-K
Citations Scopus - 8Web of Science - 8
1998 Mattes J, Karmaus W, Moseler M, Frischer T, Kuehr J, 'Accumulation of atopic disorders within families: a sibling effect only in the offspring of atopic fathers', CLINICAL AND EXPERIMENTAL ALLERGY, 28 1480-1486 (1998)
Citations Scopus - 21Web of Science - 24
Show 113 more journal articles

Conference (89 outputs)

Year Citation Altmetrics Link
2020 Platt L, Pearce K, Goddard B, Belinelo DGP, Roddick L, Hilton J, et al., 'JOHN HUNTER CHILDREN'S HOSPITAL (JHCH) SEVERE ASTHMA CLINIC (SAC) - THE DIAGNOSTIC APPROACH', RESPIROLOGY (2020)
Co-authors Adam Collison
2020 Wood L, Berthon B, Mcloughlin R, Jensen M, Hosseini B, Williams E, et al., 'INTERVENTION WITH A HIGH FRUIT AND VEGETABLE DIET IMPROVES LUNG FUNCTION AND DECREASES ASTHMA RELATED ILLNESS IN CHILDREN WITH ASTHMA', RESPIROLOGY (2020)
Co-authors Adam Collison, Peter Wark
2020 Hosseini B, Wark P, Berthon B, Williams E, Mcloughlin R, Jensen M, et al., 'INCREASING FRUIT AND VEGETABLE INTAKE MODIFIES INNATE IMMUNE RESPONSES IN CHILDREN WITH ASTHMA', RESPIROLOGY (2020)
Co-authors Peter Wark, Adam Collison
2020 Hosseini B, Wark P, Berthon B, Williams E, Mcloughlin R, Jensen M, et al., 'CHILDREN WITH ASTHMA HAVE IMPAIRED INNATE IMMUNE RESPONSES COMPARED WITH HEALTHY CONTROLS', RESPIROLOGY (2020)
Co-authors Peter Wark, Adam Collison
2019 Woolard A, Benders T, Campbell L, Karayanidis F, Murphy V, Lane S, et al., 'The relationship between pitch contours in infant-directed speech and infant risk for autism.', International Society for Autism Research Annual Meeting, Montreal, Canada. (2019)
Co-authors Alison Lane, Vanessa Murphy, Frini Karayanidis, Linda E Campbell, Alix Woolard Uon
2019 Gomes GMC, Belinelo PG, Starkey MR, Jesson K, Loering S, Hansbro PM, et al., 'Unique subpopulations of cord blood innate lymphoid cells are associated with lung function at 6 weeks of age in babies born to mothers with asthma during pregnancy', ALLERGY, Lisbon, PORTUGAL (2019)
Co-authors Adam Collison, Vanessa Murphy, Peter Gibson, Malcolm Starkey
2019 Belinelo PDG, Jesson K, Appenzeller R, Gorlanova O, Collison A, Oldmeadow C, et al., 'Late Breaking Abstract - Maternal asthma, weight gain in early life and infant lung function', EUROPEAN RESPIRATORY JOURNAL, Madrid, SPAIN (2019)
DOI 10.1183/13993003.congress-2019.OA4937
Co-authors Peter Gibson, Adam Collison, Vanessa Murphy, Christopher Oldmeadow
2019 Andrade EDQY, Murphy V, Belinelo PDG, Jesson K, Collison A, Robinson P, et al., 'Prematurity and respiratory function at 6 weeks of age in infants born to mothers with asthma during pregnancy and active tobacco smoking', EUROPEAN RESPIRATORY JOURNAL, Madrid, SPAIN (2019)
DOI 10.1183/13993003.congress-2019.PA309
Co-authors Peter Gibson, Adam Collison, Vanessa Murphy
2019 Harvey S, Murphy V, Gibson P, Mattes J, Collison A, Jensen M, 'The association between breastfeeding and respiratory health in infants born to women with asthma: a secondary analysis of two cohort studies', EUROPEAN RESPIRATORY JOURNAL, Madrid, SPAIN (2019)
DOI 10.1183/13993003.congress-2019.PA5003
Citations Web of Science - 1
Co-authors Adam Collison, Peter Gibson, Megan Jensen, Vanessa Murphy
2019 Murphy VE, Jensen M, Robijn A, Wright T, Mattes J, Collison A, Gibson P, 'Influence of maternal body mass index and gestational weight gain, with asthma management on maternal and infant outcomes', EUROPEAN RESPIRATORY JOURNAL, Madrid, SPAIN (2019)
DOI 10.1183/13993003.congress-2019.PA5026
Co-authors Adam Collison, Peter Gibson, Megan Jensen, Vanessa Murphy
2019 Wark P, Nichol K, Dorahy D, Collison A, Mattes J, 'Treatment with Omalizumab in adults with severe allergic reduces Fc?I expression on dendritic cells and improves antiviral responses', EUROPEAN RESPIRATORY JOURNAL, Madrid, SPAIN (2019)
DOI 10.1183/13993003.congress-2019.PA534
Co-authors Adam Collison, Peter Wark
2018 Wark P, Nichol K, Dorahy D, Collison A, Mattes J, 'THE EFFECT OF TREATMENT WITH OMALIZUMAB ON ANTIVIRAL RESPONSES IN ADULTS WITH SEVERE ALLERGIC ASTHMA', RESPIROLOGY (2018)
Co-authors Adam Collison, Peter Wark
2018 Belinelo PDG, Nielsen A, Goddard B, Collison AM, Robinson PD, Whitehead B, et al., 'Nitrogen (N2) multiple breath washout: Assessment of ventilation inhomogeneity in severe paediatric asthma', EUROPEAN RESPIRATORY JOURNAL, Paris, FRANCE (2018)
DOI 10.1183/13993003.congress-2018.PA1316
Co-authors Adam Collison
2018 Gomes GMC, Belinelo PDG, Malcolm RS, Jesson K, Phil MH, Vanessa EM, et al., 'Cord blood eosinophils and Type 2 Innate lymphoid cells are correlated in infants born to mothers with asthma during pregnancy', EUROPEAN RESPIRATORY JOURNAL, Paris, FRANCE (2018)
DOI 10.1183/13993003.congress-2018.PA5433
Co-authors Vanessa Murphy, Adam Collison, Philip Hansbro, Peter Gibson, Malcolm Starkey
2018 Wark PAB, Nichol K, Dorahy D, Collison A, Mattes J, 'The Effect of Treatment with Omalizumab on Anti-Viral Responses in Adults with Severe Allergic Asthma', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, San Diego, CA (2018)
Co-authors Adam Collison, Peter Wark
2018 Lane A, Campbell L, Gibson P, Woolard A, Barker D, Tait J, et al., 'Early signs of autism in 12 month infants born to mothers with asthma', Griffith University, Gold Coast (2018)
Co-authors Linda E Campbell, Adam Collison, Frini Karayanidis, Alison Lane, Alix Woolard Uon, Peter Gibson, Vanessa Murphy
2018 Nielsen A, Belinelo DGP, Goddard B, Collison A, Robinson P, Whitehead B, et al., 'LUNG CLEARANCE INDEX AS A MARKER OF SEVERE ASTHMA IN A PAEDIATRIC POPULATION', RESPIROLOGY (2018)
Co-authors Adam Collison
2018 Beinelo DGP, Jesson K, Sena SC, Collison A, Murphy V, Robinson P D, et al., 'LUNG FUNCTION AT 6 WEEKS OF AGE IS ASSOCIATED WITH THE RISK OF DEVELOPING BRONCHIOLITIS IN INFANTS BORN TO MOTHERS WITH ASTHMA DURING PREGNANCY', RESPIROLOGY (2018)
Co-authors Adam Collison, Vanessa Murphy, Peter Gibson
2018 Jesson K, Belinelo DGP, Sena C RS, Collison A, Murphy V, Robinson P, et al., 'PREMATURITY, LUNG FUNCTION AT 6 WEEKS OF AGE AND BRONCHIOLITIS IN BABIES BORN TO MOTHERS WITH ASTHMA DURING PREGNANCY', RESPIROLOGY (2018)
Co-authors Peter Gibson, Vanessa Murphy, Adam Collison
2018 Gomes G, Starkey M, Belinelo DGP, Jesson K, Hansbro P, Murphy V, et al., 'PROFILING INNATE LYMPHOID CELLS IN THE CORD BLOOD OF INFANTS BORN TO MOTHERS WITH ASTHMA IN PREGNANCY', RESPIROLOGY (2018)
Co-authors Philip Hansbro, Vanessa Murphy, Adam Collison, Peter Gibson
2017 Perkes S, Gruppetta M, Bonevski B, Mattes J, Gould G, 'Mothers Aunties Maternal Aboriginal Smokers (MAMAS) Study', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2017)
Co-authors Billie Bonevski, Gillian Gould
2017 Tay HL, Hsu A, Nguyen T, Donovan C, Collison A, Mattes J, et al., 'Interleukin-36 gamma: Roles in lungs innate immunity, inflammation and allergy', CYTOKINE, Int Cytokine & Interferon Soc, Kanazawa, JAPAN (2017)
Co-authors Chantal Donovan, Paul Foster, Adam Collison, Alan Hsu, Gerard Kaiko, Ming Yang, Philip Hansbro, Hock Tay
2017 Morten M, Collison A, Murphy V, Barker D, Meredith J, Powell H, et al., 'ASTHMA CONTROL DURING PREGNANCY, 17Q21 VARIANTS AND CHILDHOOD-ONSET ASTHMA', RESPIROLOGY (2017)
Citations Web of Science - 1
Co-authors Adam Collison, Vanessa Murphy, Peter Gibson, Daniel Barker
2017 Collison A, Li J, De Siqueira AP, Lv X, Toop HD, Morris JC, et al., 'THE E3 UBIQUITIN LIGASE MID1 PROMOTES IDIOPATHIC PULMONARY FIBROSIS', RESPIROLOGY (2017)
Co-authors Adam Collison, Malcolm Starkey, Philip Hansbro
2017 Belinelo PDG, Jesson K, Collison A, Murphy V, Robinson P, Hardaker K, et al., 'Respiratory Function at 6 weeks of age is associated with the development of bronchiolitis in infants born to mothers with asthma during pregnancy', EUROPEAN RESPIRATORY JOURNAL, Milan, ITALY (2017)
DOI 10.1183/1393003.congress-2017.OA3444
Co-authors Adam Collison
2016 Jensen ME, Camargo CA, Gibson PG, Mattes J, Murphy VE, 'Maternal Serum Ditamin D Levels \= 75nmol/l During Pregnancy Are Associated With Fewer Adverse Respiratory Outcomes In Infants At 12 Months Of Age', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, San Francisco, CA (2016)
Co-authors Megan Jensen, Vanessa Murphy, Peter Gibson
2016 Jensen M, Murphy V, Mattes J, Gibson P, Carmargo JC, 'MATERNAL SERUM VITAMIN D LEVELS \= 75 NMOL/L DURING PREGNANCY ARE ASSOCIATED WITH FEWER ADVERSE RESPIRATORY OUTCOMES IN INFANTS AT 12 MONTHS OF AGE', RESPIROLOGY (2016)
Co-authors Vanessa Murphy, Peter Gibson
2016 Kepreotes E, Whitehead B, Lee M, Collison A, Goddard B, Cheese L, et al., 'HIGH-FLOW OXYGEN COMPARED TO STANDARD NASAL CANNULA OXYGEN DOES NOT REDUCE THE MEDIAN TIME ON OXYGEN FOR INFANTS WITH MODERATE BRONCHIOLITIS', RESPIROLOGY (2016)
Co-authors Christopher Oldmeadow, Adam Collison, John Attia
2016 Horvat J, Kim R, Pinkerton J, Rae B, Starkey M, Essilfie A, et al., 'IDENTIFICATION OF NOVEL THERAPEUTIC TARGETS FOR STEROID-INSENSITIVE ASTHMA USING MODELS THAT REPRESENT DIFFERENT CLINICAL SUBTYPES OF DISEASE', RESPIROLOGY (2016)
Co-authors Philip Hansbro, Simon Keely, Jay Horvat
2016 Murphy V, Gibson PG, Collison A, Sly P, Czovek D, Robinson P, et al., 'Follow-up of infants from the Breathing for Life Trial BLT Babies and BLT-Infant Development.', Perinatal Society IMPACT Workshop, Townsville. (2016)
Co-authors Vanessa Murphy, Frini Karayanidis, Linda E Campbell, Alison Lane
2016 Rhys-Jones B, Rowland A, Hankin R, Hilton J, Whitehead B, Kumar R, Mattes J, 'QUANTIFICATION OF LUNG FUNCTION ABNORMALITY IN INFANTS WITH CONGENITAL THORACIC MALFORMATIONS AFTER SURGICAL RESECTION IN EARLY LIFE', RESPIROLOGY (2016)
2016 Mandaliya P, Kennedy B, Fitzgerald D, Selvadurai H, Karpelowsky J, Harvey J, et al., 'RESPIRATORY FUNCTION ABNORMALITIES ARE COMMON AT SCHOOL AGE IN CHILDREN OPERATED ON FOR CONGENITAL THORACIC MALFORMATION (CTM) IN INFANCY', RESPIROLOGY (2016)
2016 Kepreotes E, Whitehead B, Attia J, Oldmeadow C, Collison A, Goddard B, et al., 'A randomized controlled trial examining high-flow oxygen in the management of infants with moderate bronchiolitis', EUROPEAN RESPIRATORY JOURNAL (2016)
DOI 10.1183/13993003.congress-2016.OA4983
Co-authors John Attia, Christopher Oldmeadow, Adam Collison
2016 Morten M, Collison A, Meredith J, Murphy V, Robinson P, Gibson P, Mattes J, 'FeNO-guided management of asthma during pregnancy reduces respiratory symptoms and asthma diagnosis in childhood', EUROPEAN RESPIRATORY JOURNAL (2016)
DOI 10.1183/13993003.congress-2016.PA330
Co-authors Adam Collison
2016 Horvat J, Kim R, Pinkerton J, Rae B, Starkey M, Essilfie A-T, et al., 'Identification of therapeutic targets for steroid-insensitive asthma using models that represent different clinical subtypes of disease', EUROPEAN RESPIRATORY JOURNAL (2016)
DOI 10.1183/13993003.congress-2016.PA563
Co-authors Simon Keely, Paul Foster, Philip Hansbro, Jay Horvat
2016 Meredith J, Morten M, Kepreotes E, Collison A, Mattes J, 'Lung function determined by impulse oscillometry in preschoolers hospitalised for moderate or severe bronchiolitis in infancy', EUROPEAN RESPIRATORY JOURNAL (2016)
DOI 10.1183/13993003.congress-2016.PA4365
Co-authors Adam Collison
2016 Woolard A, Benders T, Campbell L, Karayanidis F, Mattes J, Murphy V, et al., 'Exploring the association of infant temperament on maternal fundamental frequency contours.', Proceedings of the Sixteenth Australasian International Conference on Speech Science and Technology, University of Western Sydney, Parramatta (2016)
Co-authors Alison Lane, Linda E Campbell, Frini Karayanidis, Alix Woolard Uon, Vanessa Murphy
2016 Collison A, Sokulsky LA, Starkey MR, Nightingale S, Le Fevre A, Percival E, et al., 'TRAIL regulates egg-allergen induced eosinophilic oesophagitis', EUROPEAN JOURNAL OF IMMUNOLOGY, Melbourne, AUSTRALIA (2016)
Co-authors Malcolm Starkey, Adam Collison, Paul Foster, Philip Hansbro
2015 roche J, hunter S, Stokes-Parish J, Lovett S, Mattes J, 'Students as Peer Assessors in Simulation.', Newcastle, NSW (2015)
Co-authors Sharyn Hunter, Jessica Stokes
2015 Kim R, Horvat J, Pinkerton J, Starkey M, Essilfie A, Mayall J, et al., 'INFECTION-INDUCED MICRORNA-21 DRIVES SEVERE, STEROID-INSENSITIVE EXPERIMENTAL ASTHMA BY AMPLIFYING PI3K-MEDIATED SUPPRESSION OF HDAC2', RESPIROLOGY, Queensland, AUSTRALIA (2015) [E3]
Co-authors Jemma Mayall, Jay Horvat, Malcolm Starkey, Philip Hansbro, Paul Foster, Simon Keely
2015 Tay H, Kaiko G, Plank M, Li J, Essilfie A, Maltby S, et al., 'THE ROLE OF MIR-328 IN RESPIRATORY DISEASES', RESPIROLOGY, Queensland, AUSTRALIA (2015) [E3]
Co-authors Steven Maltby, Ming Yang, Gerard Kaiko, Philip Hansbro, Paul Foster, Hock Tay
2015 Lum S, Bountziouka V, Wade A, Kirkby J, De Mir I, Mattes J, et al., 'New reference equations for interpreting results from the raised volume technique (RVRTC) in infants', EUROPEAN RESPIRATORY JOURNAL (2015)
DOI 10.1183/13993003.congress-2015.OA3499
2015 Lum S, Bountziouka V, Wade A, Kirkby J, Moreno-Galdo A, Sardon Prado O, et al., 'Equipment specific reference ranges for the raised volume technique (RVRTC) in infants: A multi-centre collaboration', EUROPEAN RESPIRATORY JOURNAL (2015)
DOI 10.1183/13993003.congress-2015.PA1261
2015 Collison AM, Sokulsky LA, Sherrill JD, Nightingale S, Hatchwell L, Talley NJ, et al., 'TRAIL Signalling Is Pro-Inflammatory in Eosinophilic Esophagitis', JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Houston, TX (2015) [E3]
DOI 10.1016/j.jaci.2014.12.1185
Co-authors Nicholas Talley, Adam Collison, Marjorie Walker
2015 Hansbro P, Kim R, Pinkerton J, Starkey M, Essilfie A-T, Mayall J, et al., 'MicroRNA-21 drives severe, steroid-insensitive experimental asthma by amplifying PI3K-mediated suppression of HDAC2', JOURNAL OF IMMUNOLOGY, New Orleans, LA (2015)
Co-authors Paul Foster, Simon Keely, Jay Horvat, Philip Hansbro
2015 Tay H, Kaiko G, Mattes J, Hansbro P, Foster P, 'The role of miR-328 in respiratory diseases', JOURNAL OF IMMUNOLOGY, New Orleans, LA (2015)
Co-authors Paul Foster, Philip Hansbro, Gerard Kaiko
2015 Hansbro P, Haw T, Nair P, Hanish I, Nguyen D, Liu G, et al., 'Tumour necrosis factor-related apoptosis inducing ligand promotes the development of experimental chronic obstructive pulmonary disease', JOURNAL OF IMMUNOLOGY, New Orleans, LA (2015)
Co-authors Jay Horvat, Adam Collison, Philip Hansbro, Darryl Knight
2015 Hansbro PM, Kim RY, Pinkerton JW, Starkey MR, Essilfie AT, Mayall JR, et al., 'Infection-Induced Microrna-21 Drives Severe, Steroid-Insensitive Experimental Asthma By Amplifying PhosphoINOSitide-3-Kinase (pi3k)-Mediated Suppression Of Histone Deacetylase (hdac)2', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Denver, CO (2015)
Co-authors Paul Foster, Simon Keely, Philip Hansbro, Malcolm Starkey, Jay Horvat
2015 Percival E, Bhatia R, McElduff P, McEvoy M, Collison A, Mattes J, 'REPRODUCIBILITY OF ARA h2 SKIN PRICK TESTING AND FRACTION OF EXHALED NITRIC OXIDE IN THE ASSESSMENT OF PAEDIATRIC PEANUT ALLERGY', INTERNAL MEDICINE JOURNAL (2015) [E3]
Co-authors Patrick Mcelduff, Adam Collison, Mark Mcevoy
2014 Mandaliya PH, Bhatia R, Belcher J, McElduff P, Collison A, Mattes J, 'Is fraction of exhaled nitric oxide (FeNO) able to predict severity of allergic reaction at an open cooked egg challenge?', ALLERGY, Copenhagen, DENMARK (2014) [E3]
Co-authors Adam Collison, Patrick Mcelduff
2014 Collison A, Hatchwell L, Girkin J, Parsons K, Li J, Zhang J, et al., 'Late-breaking abstract: IL-5-induced airways eosinophilia as a negative regulator of TLR7 expression may impair the interferon response to rhinovirus in allergic airways', EUROPEAN RESPIRATORY JOURNAL (2014)
Co-authors Paul Foster, Jason Girkin, Adam Collison, Peter Wark, Nathan Bartlett
2014 Mandaliya PH, Morten M, Kumar R, James A, Whitehead B, Platt L, et al., 'Lung Clearance Index (lci) May Be More Sensitive In Detecting Residual Lung Function Abnormalities In Children Operated For Suspected Congenital Cystic Adenomatoid Malformation In Infancy', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2014)
Co-authors Aniruddh Deshpande
2014 Rhys-Jones B, Rowland A, Hankin R, Hilton J, Kumar R, Whitehead B, Mattes J, 'Infants Who Underwent Surgery For Congenital Lung Lesions In Early Life Have Impaired Fev0.5 And FVC Values As Compared To Healthy Infants', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2014)
2014 Collison A, Hatchwell L, Girkin J, Li J, Parsons K, Bartlett N, et al., 'REDUCED TLR7 EXPRESSION MAY UNDERPIN IMPAIRED RESPONSE TO VIRAL INFECTION IN ASTHMA', RESPIROLOGY (2014) [E3]
DOI 10.1111/resp.12263_5
Co-authors Adam Collison, Peter Wark, Paul Foster, Jason Girkin
2014 Li J, Collison A, De Siqueira PA, Zhang J, Mattes J, 'TUMOUR NECROSIS FACTOR RELATED APOPTOSIS INDUCING LIGAND (TRAIL) REGULATION OF PROTEIN PHOSPHATASE (PP)2A IS CRUCIAL FOR THE DEVELOPMENT OF BLEOMYCIN INDUCED PULMONARY FIBROSIS IN MICE', RESPIROLOGY (2014) [E3]
Co-authors Adam Collison
2014 Preece K, Bhatia R, Belcher J, Patchett K, Mcelduff P, Collison A, Mattes J, 'FRACTION OF EXHALED NITRIC OXIDE IS A NOVEL NON-INVASIVE PREDICTOR OF PEANUT ALLERGY', RESPIROLOGY (2014) [E3]
Co-authors Patrick Mcelduff, Adam Collison
2014 Rhys-Jones B, Bhatia R, Hilton J, Kumar R, Mattes J, 'RECURRENT, THERAPY-RESISTANT ALVEOLAR INFILTRATES IN A YOUNG CHILD: APPROACHES TO DIAGNOSIS AND CHALLENGES IN MANAGEMENT', RESPIROLOGY (2014) [E3]
2014 Girkin J, Sokulsky L, Hatchwell L, Starkey M, Collison A, Hansbro P, Mattes J, 'IDENTIFICATION OF A NOVEL INTERLEUKIN-13 SIGNALLING PATHWAY', RESPIROLOGY (2014) [E3]
Co-authors Jason Girkin, Adam Collison, Malcolm Starkey, Philip Hansbro
2013 Kumar RK, Collison A, Siegle JS, Hansbro NG, Kwok C-T, Herbert C, et al., 'Epigenetic Changes Associated With Disease Progression In A Model Of Childhood Allergic Asthma', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2013)
Co-authors Nicole Hansbro, Adam Collison, Paul Foster
2013 Preece KD, Bhatia R, Belcher J, Patchett K, McElduff P, Mattes J, 'Prospective validation and accuracy of Ara h2 in the diagnosis of childhood peanut allergy', ALLERGY, Milan, ITALY (2013) [E3]
Co-authors Patrick Mcelduff
2013 Lovett, Roche J, Hunter S, Symonds I, Mattes J, 'Medical students' clinical reasoning development during simulation', Prato, Italy (2013)
Co-authors Sharyn Hunter
2013 Girkin J, Hatchwell L, Foster PS, Johnston SL, Collison A, Mattes J, 'SALMETEROL ATTENUATES CHEMOTAXIS IN RHINOVIRUS-INDUCED EXACERBATION OF ASTHMA VIA MODULATION OF PP2A', RESPIROLOGY (2013) [E3]
Co-authors Jason Girkin, Adam Collison, Paul Foster
2013 Mattes J, Murphy V, Powell H, Gibson P, 'THE EFFECT OF BETTER ASTHMA CONTROL IN PREGNANCY ON WHEEZY ILLNESSES IN INFANCY', RESPIROLOGY (2013) [E3]
Citations Web of Science - 2
Co-authors Peter Gibson, Vanessa Murphy
2013 Gunawardhana LP, Baines KJ, Mattes J, Murphy VE, Simpson JL, Gibson PG, 'EPIGENETIC ALTERATIONS IN INFANTS ASSOCIATED WITH MATERNAL ASTHMA DURING PREGNANCY', RESPIROLOGY (2013) [E3]
Co-authors Katherine Baines, Peter Gibson, Jodie Simpson, Vanessa Murphy
2013 Hatchwell L, Collison A, Phipps S, Foster PS, Johnston SL, Mattes J, 'CCL7 (MCP-3) MEDIATES RHINOVIRUS-INDUCED LUNG INFLAMMATION AND EXACERBATION OF ALLERGIC AIRWAY DISEASE', RESPIROLOGY (2013) [E3]
Co-authors Paul Foster, Adam Collison
2012 Starkey M, Kim R, Horvat J, Essilfie A-T, Beagley K, Mattes J, et al., 'Constitutive IL-13 promotes respiratory chlamydial infection and infection-induced chronic airway hyper-responsiveness', JOURNAL OF IMMUNOLOGY, Boston, MA (2012) [E3]
Co-authors Philip Hansbro, Paul Foster, Jay Horvat
2012 Collison AM, Hatchwell LM, Siqueira AP, Bartlett NW, Johnston SL, Foster PS, Mattes J, 'Antagonism of microRNA-122 is comparible to azithromycin treatment in a mouse model of rhinovirus-induced exacerbation of allergic airways disease', Respirology, Canberra, ACT (2012) [E3]
Co-authors Paul Foster, Adam Collison, Nathan Bartlett
2012 Hatchwell LM, Collison AM, Siqueira AP, Bartlett NW, Johnston SL, Foster PS, Mattes J, 'Toll-like receptor 7 mediates anti-viral responses to rhinovirus while suppressing exacerbation of asthma', Respirology, Canberra, ACT (2012) [E3]
Co-authors Nathan Bartlett, Paul Foster, Adam Collison
2012 Hatchwell LM, Collison AM, Siqueira AP, Bartlett NW, Johnston SL, Foster PS, Mattes J, 'TRAIL regulates inflammatory responses to rhinovirus and rhinovirus-induced exacerbation of asthma', Respirology, Canberra, ACT (2012) [E3]
Co-authors Adam Collison, Nathan Bartlett, Paul Foster
2012 Plank MW, Kaiko GE, Luck H, Li J, Mattes J, Hansbro PM, Foster PS, 'The role of micrornas in CD4 T cell function', Respirology, Canberra, ACT (2012) [E3]
Co-authors Philip Hansbro, Gerard Kaiko, Paul Foster
2012 Starkey MR, Kim RY, Horvat JC, Essilfie A-T, Beagley KW, Mattes J, et al., 'Constitutive IL-13 promotes respiratory chlamydial infection-induced chronic airway hyperresponsiveness', Respirology, Canberra, ACT (2012) [E3]
Co-authors Malcolm Starkey, Philip Hansbro, Jay Horvat, Paul Foster
2012 Tay HL, Kaiko GE, Plank MW, Mattes J, Hansbro PM, Foster PS, 'MiRNAs regulate bacterial infection in lungs', Respirology, Canberra, ACT (2012) [E3]
Co-authors Gerard Kaiko, Hock Tay, Philip Hansbro, Paul Foster
2011 Foster PS, Tay HL, Kaiko GE, Plank MW, Mattes J, Hansbro PM, 'MiRNA and its roles in regulating bacterial infection in lungs', American Journal of Respiratory and Critical Care Medicine, Denver, CO (2011) [E3]
Co-authors Paul Foster, Hock Tay, Gerard Kaiko, Philip Hansbro
2011 McLaughlin KM, Mattes J, Murphy VE, Steel KR, Powell H, Gibson PG, 'The Growing Into Asthma (GIA) Study: Need for improved management of respiratory illnesses in early life', PSANZ 2011 15th Annual Congress: Poster Abstracts, Hobart, TAS (2011) [E3]
Co-authors Vanessa Murphy, Karen Mclaughlin, Peter Gibson
2011 Gunawardhana LP, Baines KJ, Simpson JL, Mattes J, Murphy VE, Gibson PG, 'Maternal asthma is associated with alterations in DNA methylation profile of peripheral blood of infants', Respirology, Perth, WA (2011) [E3]
Co-authors Vanessa Murphy, Jodie Simpson, Katherine Baines, Peter Gibson
2011 Mattes J, Murphy VE, McLaughlin KM, Steel KR, Powell H, Gibson PG, 'Are maternal asthma exacerbations during pregnancy related to impaired infant growth in the first six months of life?', Respirology, Perth, WA (2011) [E3]
Co-authors Karen Mclaughlin, Vanessa Murphy, Peter Gibson
2011 Collison AM, Hatchwell LM, Pereira De Siqueira AL, Don A, Verrills NM, Foster PS, Mattes J, 'The development of house dust mite-induced allergic airways disease is regulated by a novel E3 ubiquitin ligase-dependent deactivation of a protein phosphatase', Respirology, Perth, WA (2011) [E3]
Co-authors Adam Collison, Nikki Verrills, Paul Foster
2011 Hatchwell LM, Collison AM, Pereira De Siqueira AL, Foster PS, Verrills NM, Don A, et al., 'A novel E3 ubiquitin ligase links rhinovirus infection to exacerbation of asthma', Respirology, Perth, WA (2011) [E3]
Co-authors Paul Foster, Nikki Verrills, Adam Collison, Peter Wark
2011 Mattes J, Hankin RG, Hilton JM, Collison AM, Pereira De Siqueira AL, Gulliver T, et al., 'Frequent persistent wheeze in infancy may be associated with impaired FEV0.5 and FVC values', Respirology, Perth, WA (2011) [E3]
Citations Web of Science - 1
Co-authors Paul Foster, Adam Collison
2010 Ptaschinski CM, Phipps S, Hansbro NG, Rosenberg HF, Mattes J, Foster PS, 'MicroRNAs are involved in the regulation of inflammatory responses characteristic of severe respiratory virus infection', American Journal of Respiratory and Critical Care Medicine, New Orleans (2010) [E3]
Co-authors Paul Foster, Nicole Hansbro
2010 Mattes J, Collison AM, Plank MW, Phipps S, Foster PS, 'The role of microRNA as new anti-inflammatory targets', APCAACI 2010: The 8th Asia Pacific Congress on Allergy, Asthma and Clinical Immunology Programme & Abstracts Handbook, Singapore (2010) [E3]
Co-authors Adam Collison, Paul Foster
2010 Foster PS, Mattes J, Collison AM, Plank MW, Phipps S, 'MicoRNAs bridge innate and adative immunity: induction of TH2 mediated allergic airways disease', OzBio 2010: The Molecules of Life - from Discovery to Biotechnology. Abstracts, Melbourne, Vic (2010) [E3]
Co-authors Adam Collison, Paul Foster
2009 Collison AM, Mattes J, Phipps S, Plank MW, Foster PS, 'MicroRNAs are crucial in the development of airways hyperreactivity', American Journal of Respiratory and Critical Care Medicine, San Diego, CA (2009) [E3]
Co-authors Paul Foster, Adam Collison
2009 Mattes J, Collison AM, Plank MW, Phipps S, Foster PS, 'MicroRNAs regulate allergic airway inflammation', American Journal of Respiratory and Critical Care Medicine, San Diego, CA (2009) [E3]
Co-authors Adam Collison, Paul Foster
2009 Collison AM, De Siqueira A, Plank MW, Foster PS, Mattes J, 'The identification of TRAIL as a mediator of airways remodelling in a chronic model of murine allergic airways disease', American Journal of Respiratory and Critical Care Medicine, San Diego, CA (2009) [E3]
Co-authors Adam Collison, Paul Foster
2007 Talbot PI, Wright IM, Hilton JM, Mattes J, Clifton VL, 'Effect of maternal asthma during pregnancy on childhood growth and development of atopic disease', Respirology (TSANZ Abstracts-Posters), Auckland (2007) [E3]
Co-authors Ian Wright
2006 Mattes J, Simpson JL, Foster PS, Gibson PG, 'Trail is upregulated in the airways of asthmatics', Respirology, Canberra (2006) [E3]
Co-authors Paul Foster, Jodie Simpson, Peter Gibson
2002 Klysner S, Mahalingam S, Neisig A, Hertz M, Dalum I, Mattes J, et al., 'Induction of a protective immune response in a murine model of asthma by DNA vaccination with modified IL-5', ALLERGY, NAPLES, ITALY (2002)
2002 Lange J, Schaefer D, Engels E, Mattes J, Kuehr J, Kopp M, 'Interferon-gamma and IL-13 production in response to PHA and IL-18 by human cord blood mononuclear cells', ALLERGY, NAPLES, ITALY (2002)
Citations Web of Science - 1
Show 86 more conferences

Other (1 outputs)

Year Citation Altmetrics Link
2019 Lane A, Van Aswegen M, Turner-Presker M, Whalen O, Mattes J, Gibson P, et al., 'Sensory correlates of autism risk in the first year of life: A multi-cohort study.', (2019) [O1]
Co-authors Vanessa Murphy, Linda E Campbell, Alison Lane, Shelly Lane
Edit

Grants and Funding

Summary

Number of grants 53
Total funding $12,662,404

Click on a grant title below to expand the full details for that specific grant.


20204 grants / $83,907

Identifying the food trigger for children with Eosinophilic Oesophagitis$40,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Adam Collison, Professor Joerg Mattes, Doctor Scott Nightingale, Professor Simon Keely
Scheme Research Grant
Role Investigator
Funding Start 2020
Funding Finish 2020
GNo G2000205
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

A randomised controlled pilot trial to determine the effect of smoking cessation during pregnancy on perinatal and infant respiratory outcomes$21,745

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Professor Joerg Mattes, Doctor Adam Collison
Scheme Research Grant
Role Lead
Funding Start 2020
Funding Finish 2020
GNo G2000634
Type Of Funding C3112 - Aust Not for profit
Category 3112
UON Y

Preschool age follow-up for the breathing for life trial (BLT) a longitudinal birth cohort study following children of asthmatic mothers$12,162

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Professor Joerg Mattes, Doctor Adam Collison
Scheme Research Grant
Role Lead
Funding Start 2020
Funding Finish 2020
GNo G2000399
Type Of Funding C3112 - Aust Not for profit
Category 3112
UON Y

Investigating the health effects of bushfire smoke exposure, specifically on people with asthma, including pregnant women with asthma, and their children$10,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Conjoint Professor Peter Gibson, Doctor Vanessa Murphy, Professor Vanessa McDonald, Doctor Adam Collison, Conjoint Associate Professor Anne Vertigan, Doctor Megan Jensen, Doctor Dennis Thomas, Associate Professor Jay Horvat, Professor Maralyn Foureur, Professor Leigh Kinsman, Associate Professor Liz Holliday, Doctor Erin Harvey, Ms Alycia Jacob, Professor Joerg Mattes, Graeme Zosky, Wilfried Karmaus, Michele Goldman, Dr Craig Dalton
Scheme Research Grant
Role Investigator
Funding Start 2020
Funding Finish 2020
GNo G2000414
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

20192 grants / $42,459

Development of a mobile health app for Aboriginal women and children post birth to five years, including smoking cessation$29,959

Funding body: NSW Agency for Clinical Innovation (ACI)

Funding body NSW Agency for Clinical Innovation (ACI)
Project Team Professor Billie Bonevski, Professor Joerg Mattes, Miss Sarah Perkes, Dr Kerry Hall, Jill Branford, Lee-Anne Brogmus, Lee-Anne Brogmus , Noelene Skinner
Scheme Research Project
Role Investigator
Funding Start 2019
Funding Finish 2019
GNo G1801296
Type Of Funding C2220 - Aust StateTerritoryLocal - Other
Category 2220
UON Y

Indigenous Australian maternal and child health, with a focus on respiratory health $12,500

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Miss Sarah Perkes, Professor Billie Bonevski, Professor Joerg Mattes, Dr Kerry Hall
Scheme Postgraduate Research Scholarship
Role Investigator
Funding Start 2019
Funding Finish 2021
GNo G1901486
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

20181 grants / $25,000

Immunological mechanisms in the primary prevention of asthma$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Adam Collison, Professor Joerg Mattes, Doctor Malcolm Starkey
Scheme Project Grant
Role Investigator
Funding Start 2018
Funding Finish 2018
GNo G1801259
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

20174 grants / $2,407,623

'Indigenous Counselling and Nicotine (ICAN) QUIT in Pregnancy' - a cluster randomised trial to implement culturally competent evidence-based smoking cessation for pregnant Aboriginal and Torres Strait$2,347,623

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Associate Professor Gillian Gould, Professor Billie Bonevski, Prof Katherine Boydell, A / Prof Kristin Carson, Assoicate Professor Alan Clough, Professor Chris Doran, Professor Joerg Mattes, Doctor Christopher Oldmeadow, Mrs Marilyn Clarke, Professor Peter O'Mara, Laureate Professor Roger Smith
Scheme Global Alliance for Chronic Diseases
Role Investigator
Funding Start 2017
Funding Finish 2021
GNo G1501260
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

The role of microbiome development in the early origins of asthma in a high risk population$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Adam Collison, Professor Joerg Mattes
Scheme Project Grant
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1700818
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Understanding the role of diet and gut bacteria in asthmatic children$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Lisa Wood, Doctor Megan Jensen, Professor Joerg Mattes, Doctor Bronwyn Berthon, Doctor Katie Baines
Scheme Project Grant
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1701528
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Brand new assay for prediction of anaphylaxis risk$15,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Joerg Mattes, Doctor Adam Collison
Scheme Commercialisation in Medical Research Grant
Role Lead
Funding Start 2017
Funding Finish 2017
GNo G1700816
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

20154 grants / $1,291,320

The effect of asthma control during pregnancy on markers of airways inflammation and lung function in the offspring$1,135,272

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Joerg Mattes, Doctor Vanessa Murphy, Professor Peter Sly, Doctor Adam Collison, Professor Paul Robinson
Scheme Project Grant
Role Lead
Funding Start 2015
Funding Finish 2019
GNo G1400050
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

Improving diet quality to reduce risk of asthma attacks in children$120,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Lisa Wood, Professor Joerg Mattes, Conjoint Professor Peter Wark, Doctor Katie Baines, Doctor Megan Jensen
Scheme Project Grant
Role Investigator
Funding Start 2015
Funding Finish 2016
GNo G1500957
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Viral infections in the BLT cohort in the first year of life$19,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Joerg Mattes, Doctor Vanessa Murphy, Doctor Adam Collison
Scheme Project Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1500671
Type Of Funding C3112 - Aust Not for profit
Category 3112
UON Y

Lung function in early life for children with high asthma risk$17,048

Funding body: Rebecca L Cooper Medical Research Foundation Ltd

Funding body Rebecca L Cooper Medical Research Foundation Ltd
Project Team Professor Joerg Mattes, Doctor Vanessa Murphy, Doctor Adam Collison
Scheme Research Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1500704
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20146 grants / $2,479,834

The Breathing for Life Trial $1,722,020

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Doctor Vanessa Murphy, Conjoint Professor Peter Gibson, Emeritus Professor Michael Hensley, Professor Joerg Mattes, Professor Warwick Giles, Professor Michael Peek, Associate Professor Andrew Bisits, Associate Professor Leonie Callaway, Dr Helen Barrett
Scheme Project Grant
Role Investigator
Funding Start 2014
Funding Finish 2018
GNo G1300106
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

Toll-like receptor 7 and asthma $697,248

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Joerg Mattes, Laureate Professor Paul Foster, Conjoint Professor Peter Wark
Scheme Project Grant
Role Lead
Funding Start 2014
Funding Finish 2016
GNo G1300093
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

High-flow Nasal-prong Warm Humidified Oxygen Pilot Randomised Control Trial for infants aged = 24 months with moderate bronchiolitis$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Elizabeth Kepreotes, Professor Joerg Mattes
Scheme Project Grant
Role Investigator
Funding Start 2014
Funding Finish 2014
GNo G1301430
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Miltenyi Biotec GentleMACS Octo Dissociator with Heaters $23,566

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Phil Hansbro, Laureate Professor Paul Foster, Professor Darryl Knight, Professor Dirk Van Helden, Professor Joerg Mattes, Professor Jodie Simpson, Professor Lisa Wood, Professor Liz Milward, Dr NATHAN Bartlett, Professor Simon Keely, Doctor Steven Maltby, Doctor Andrew Jarnicki, Doctor Malcolm Starkey, Doctor Adam Collison, Doctor Shaan Gellatly
Scheme Equipment Grant
Role Investigator
Funding Start 2014
Funding Finish 2014
GNo G1500861
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

A descriptive observational study of infants aged < 24 months with severe bronchiolitis requiring critical care$10,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Elizabeth Kepreotes, Professor Joerg Mattes, Doctor Peter Harrigan, Conjoint Associate Professor Bruce Whitehead, Professor John Attia, Doctor Mark Lee
Scheme Critical Care and HMRI BRICs Nursing Research and Innovation Grant
Role Investigator
Funding Start 2014
Funding Finish 2014
GNo G1401451
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

European Respiratory Congress (ERS) 2014, ICM - International Congress Centre, Munich Germany, 6 - 10 September 2014$2,000

Funding body: University of Newcastle - Faculty of Health and Medicine

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Professor Joerg Mattes
Scheme Travel Grant
Role Lead
Funding Start 2014
Funding Finish 2015
GNo G1401074
Type Of Funding Internal
Category INTE
UON Y

20136 grants / $163,959

Asthma Australia Scholarship$73,959

Funding body: Asthma Australia

Funding body Asthma Australia
Project Team Professor Joerg Mattes
Scheme National Research Program (PhD Scholarship)
Role Lead
Funding Start 2013
Funding Finish 2015
GNo G1300552
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Molecular and cellular characterisation of TLR7 signalling in rhinovirus-induced asthma exacerbation$25,000

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Professor Joerg Mattes
Scheme Near Miss Grant
Role Lead
Funding Start 2013
Funding Finish 2013
GNo G1300469
Type Of Funding Internal
Category INTE
UON Y

Molecular and cellular characterisation of TLR7 signalling in rhinovirus-induced asthma exacerbation$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Joerg Mattes, Laureate Professor Paul Foster
Scheme Near Miss
Role Lead
Funding Start 2013
Funding Finish 2013
GNo G1300692
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

DP73 Digital colour and monochrome camera + cellSens software + Xcite120 fluorescence lamp illuminator$20,000

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Doctor Alan Hsu, Professor Phil Hansbro, Professor Joerg Mattes, Doctor Katie Baines, Professor Jodie Simpson, Professor Rakesh Kumar, Doctor Nicole Hansbro, Doctor Steven Maltby, Doctor Ming Yang, Doctor Gerard Kaiko, Associate Professor Jay Horvat, Professor Simon Keely, Doctor Andrew Jarnicki, Doctor Michael Fricker
Scheme Equipment Grant
Role Investigator
Funding Start 2013
Funding Finish 2013
GNo G1201186
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

Effect of better asthma management in pregnancy on antiviral responses, atopy and airways inflammation in early childhood$10,000

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Professor Joerg Mattes, Conjoint Professor Peter Gibson, Doctor Vanessa Murphy
Scheme Near Miss Grant
Role Lead
Funding Start 2013
Funding Finish 2013
GNo G1300476
Type Of Funding Internal
Category INTE
UON Y

Effect of better asthma management in pregnancy on antiviral responses, atopy and airways inflammation in early childhood.$10,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Joerg Mattes, Conjoint Professor Peter Gibson, Doctor Vanessa Murphy
Scheme Near Miss
Role Lead
Funding Start 2013
Funding Finish 2014
GNo G1300694
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20125 grants / $135,000

SpectraMax M5e Multi-Mode Microplate Reader$50,000

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Professor Phil Hansbro, Professor Joerg Mattes, Professor Rakesh Kumar, Doctor Nicole Hansbro, Doctor Ming Yang, Associate Professor Jay Horvat, Professor Simon Keely, Doctor Andrew Jarnicki, Doctor Linda Howland, Doctor Kelly Asquith
Scheme Equipment Grant
Role Investigator
Funding Start 2012
Funding Finish 2012
GNo G1100975
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

The Growing into Asthma Study: Wheezing prevalence and markers of airways inflammation in preschoolers born to mothers in asthma exacerbations in pregnancy$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Joerg Mattes, Conjoint Professor Peter Gibson, Emeritus Professor Michael Hensley, Conjoint Associate Professor Bruce Whitehead, Doctor Vanessa Murphy
Scheme Project Grant
Role Lead
Funding Start 2012
Funding Finish 2013
GNo G1200662
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

Novel molecular markers in children with eosinophilic oesophagitis – association with symptoms, oesophageal function and treatment response and role in disease pathogenesis$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Scott Nightingale, Professor Joerg Mattes, Doctor Adam Collison, Laureate Professor Nick Talley
Scheme Project Grant
Role Investigator
Funding Start 2012
Funding Finish 2013
GNo G1200661
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

Coordinated targeting of immune pathways to suppress infection-associated inflammatory diseases.$20,000

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Professor Phil Hansbro, Professor Joerg Mattes
Scheme Near Miss Grant
Role Investigator
Funding Start 2012
Funding Finish 2012
GNo G1200671
Type Of Funding Internal
Category INTE
UON Y

Molecular and cellular characterisation of TLR7 signalling for the expression of rhinovirus induced asthma exacerbation$20,000

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Professor Joerg Mattes
Scheme Near Miss Grant
Role Lead
Funding Start 2012
Funding Finish 2012
GNo G1200680
Type Of Funding Internal
Category INTE
UON Y

20114 grants / $1,313,780

Targeting microRNA (miRNA) as a unified therapeutic approach to the treatment of asthma and allergic inflammation$651,732

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Professor Joerg Mattes, Professor Rakesh Kumar
Scheme Project Grant
Role Investigator
Funding Start 2011
Funding Finish 2013
GNo G1000262
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

Molecular characterisation of TRAIL-regulated signal transduction pathways and their role in the development, persistence, and exacerbation of allergic airways disease$615,048

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Joerg Mattes, Associate Professor Nikki Verrills
Scheme Project Grant
Role Lead
Funding Start 2011
Funding Finish 2013
GNo G1000314
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

SCIREQ FlexiVentFX system + FlexiVentFX extension$45,000

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Phil Hansbro, Laureate Professor Paul Foster, Professor Joerg Mattes, Professor Simon Keely, Associate Professor Jay Horvat, Doctor Nicole Hansbro, Doctor Ming Yang, Doctor Catherine Ptaschinski, Doctor Kelly Asquith, Doctor Gough Au, Conjoint Professor Peter Wark, Laureate Professor John Aitken, Conjoint Professor Keith Jones, Laureate Professor Roger Smith, Professor Judith Black, Professor Rakesh Kumar, Professor Paul Hertzog
Scheme Equipment Grant
Role Investigator
Funding Start 2011
Funding Finish 2011
GNo G1100037
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

7th IES Syumposium, 21 - 25 June 2011, Quebec City$2,000

Funding body: University of Newcastle - Faculty of Health and Medicine

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Professor Joerg Mattes
Scheme Travel Grant
Role Lead
Funding Start 2011
Funding Finish 2012
GNo G1100834
Type Of Funding Internal
Category INTE
UON Y

20103 grants / $642,342

The role of microRNAs in the regulation of antiviral and inflammatory responses during experimental rhinovirus infection$583,500

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Joerg Mattes, Laureate Professor Paul Foster
Scheme Project Grant
Role Lead
Funding Start 2010
Funding Finish 2012
GNo G0190183
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

Buxco FinePointe software and FinePointe RC system for mice $39,000

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Professor Phil Hansbro, Professor Joerg Mattes, Doctor Nicole Hansbro, Doctor Simon Phipps, Doctor Ming Yang, Doctor Kelly Asquith, Doctor Catherine Ptaschinski, Professor Rakesh Kumar, Professor Judith Black
Scheme Equipment Grant
Role Investigator
Funding Start 2010
Funding Finish 2010
GNo G1000053
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

Molecular markers of reversible airway obstruction in early life and correlation with clinical wheezing patterns$19,842

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Joerg Mattes, Laureate Professor Paul Foster, Conjoint Associate Professor Bruce Whitehead, Doctor Ana Pereira De Siqueira
Scheme Project Grant
Role Lead
Funding Start 2010
Funding Finish 2010
GNo G0900119
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20098 grants / $733,575

Mechanisms and treatment of early life chlamydial infection and associated asthma$592,125

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Phil Hansbro, Professor Kenneth Beagley, Professor Joerg Mattes
Scheme Project Grant
Role Investigator
Funding Start 2009
Funding Finish 2011
GNo G0188845
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

Coulter counter$41,150

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Professor Phil Hansbro, Professor Joerg Mattes, Doctor Simon Phipps, Doctor Ming Yang, Doctor Nicole Hansbro, Doctor Kelly Asquith
Scheme Equipment Grant
Role Investigator
Funding Start 2009
Funding Finish 2009
GNo G0189851
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

Jaeger MasterScreen Baby Bodybox for infant lung function measurement$30,000

Funding body: Ramaciotti Foundations

Funding body Ramaciotti Foundations
Project Team Professor Joerg Mattes
Scheme Major Equipment Award
Role Lead
Funding Start 2009
Funding Finish 2009
GNo G0189323
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Growing into asthma: A birth cohort study to investigate the prenatal and development origins of asthma$24,800

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Vanessa Murphy, Professor Joerg Mattes, Conjoint Professor Peter Gibson
Scheme Project Grant
Role Investigator
Funding Start 2009
Funding Finish 2009
GNo G0189802
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

Development of novel therapeutic approaches for rhinovirus - induced asthma exacerbation$24,500

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Joerg Mattes, Laureate Professor Paul Foster, Conjoint Professor Peter Wark
Scheme Project Grant
Role Lead
Funding Start 2009
Funding Finish 2009
GNo G0189800
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

Growing into asthma: a birth cohort study to investigate the prenatal and development origins of asthma$13,500

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Vanessa Murphy, Professor Joerg Mattes, Conjoint Professor Peter Gibson
Scheme Project Grant
Role Investigator
Funding Start 2009
Funding Finish 2009
GNo G0190487
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

Small RNA molecules and Rhinovirus$5,000

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Professor Joerg Mattes
Scheme New Staff Grant
Role Lead
Funding Start 2009
Funding Finish 2009
GNo G0190605
Type Of Funding Internal
Category INTE
UON Y

American Thoracic Society Annual meeting, San Diego USA, 15 - 20 May 2009$2,500

Funding body: University of Newcastle - Faculty of Health and Medicine

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Professor Joerg Mattes
Scheme Travel Grant
Role Lead
Funding Start 2009
Funding Finish 2009
GNo G0190138
Type Of Funding Internal
Category INTE
UON Y

20082 grants / $635,375

The role of microRNAs as new anti-inflammatory targets for the treatment of asthma$600,375

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Professor Rakesh Kumar, Assoc. Prof Klaus Matthaei, Professor Joerg Mattes
Scheme Project Grant
Role Investigator
Funding Start 2008
Funding Finish 2010
GNo G0187584
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

Individually ventilated cages (IVC) and associated ventilator, holding boxes and water bottles$35,000

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Professor Phil Hansbro, Professor Joerg Mattes, Doctor Simon Phipps, Doctor Ming Yang, Doctor Nicole Hansbro, Doctor Kelly Asquith
Scheme Equipment Grant
Role Investigator
Funding Start 2008
Funding Finish 2008
GNo G0188541
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

20071 grants / $137,000

Molecular mechanisms of persistent allergic responses$137,000

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Joerg Mattes
Scheme Training (Postdoctoral) Fellowships - Health Professional Research Fellowship (Part-time)
Role Lead
Funding Start 2007
Funding Finish 2010
GNo G0186769
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

20062 grants / $540,282

PRC Priority Research Centre for Asthma & Respiratory Diseases$524,282

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Laureate Professor Paul Foster, Conjoint Professor Peter Gibson, Conjoint Professor Kenneth Beagley, Emeritus Professor Michael Hensley, Professor Phil Hansbro, Professor Joerg Mattes, Professor Alistair Sim, Conjoint Professor Peter Wark
Scheme Priority Research Centre
Role Investigator
Funding Start 2006
Funding Finish 2013
GNo G0186914
Type Of Funding Internal
Category INTE
UON Y

Role of TRAIL on development of atopic dermatitis and T helper type 2 immunity$16,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Joerg Mattes, Laureate Professor Paul Foster
Scheme Project Grant
Role Lead
Funding Start 2006
Funding Finish 2006
GNo G0186098
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

20051 grants / $2,030,948

Drug targets from new animal models$2,030,948

Funding body: CRC for Asthma

Funding body CRC for Asthma
Project Team Laureate Professor Paul Foster, Professor Phil Hansbro, Professor Joerg Mattes, Doctor Ming Yang, Dr Simon Phipps
Scheme Research Grant
Role Investigator
Funding Start 2005
Funding Finish 2011
GNo G0185860
Type Of Funding CRC - Cooperative Research Centre
Category 4CRC
UON Y
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Research Supervision

Number of supervisions

Completed9
Current7

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2019 PhD The Eosinophilc Microbiota - The Influence of Eosinophilia on the Mucosal Hostmicrobiota Homeostasis PhD (Paediatric & Child Hlth), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2017 PhD The Impact of bronchiolitis management in infancy and better asthma management during pregnancy on asthma prevalence and airways obstruction during childhood PhD (Paediatrics), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2017 PhD Respiratory Health Outcomes of Australian Indigenous Infants and Maternal Smoking Cessation PhD (Aboriginal Health Stud), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2017 PhD Smoking Cessation Treatment in Pregnant Women and its Impact on Their Offspring's Lung Function PhD (Paediatrics), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2017 PhD Immune function of children born to asthmatic mothers and its association with the development of asthma PhD (Paediatrics), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2016 PhD Risk Factors for Impaired Lung Function and the Onset of Respiratory Disease in Early Life PhD (Paediatrics), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2015 PhD Food Allergy and Anaphylaxis Predictors PhD (Paediatrics), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor

Past Supervision

Year Level of Study Research Title Program Supervisor Type
2020 PhD Cardiac Development and Remodeling in Preterm Infants PhD (Paediatrics), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2018 PhD Novel Approaches for the Management of Lung Disease in Children PhD (Paediatrics), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2017 PhD The Role of Trail-Regulated Signalling Pathways and TLR7 in Rhinovirus-Induced Exacerbation of Allergic Airways Disease PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2017 PhD The Role of Rhinovirus and Novel Molecular Mechanisms in Allergic Airways Disease PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2017 PhD A Novel Role for the TRAIL Signalling Pathway in the Pathogenesis of Eosinophilic Oesophagitis PhD (Paediatrics), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2017 PhD Understanding the Mechanisms of Bacterial-Induced Exacerbation of Allergic Airways Disease in a Mouse Model PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2014 PhD The Role of microRNAs in Allergic Airways Disease and T Cell Biology PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2014 PhD The Role of MicroRNA in Regulating Anti-Bacterial Responses in Innate Immune Cells PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2012 PhD Novel Therapeutic Approaches for the Treatment of Allergic Airways Disease PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
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News

New study: childhood asthma rates reduced with tailored intervention

May 16, 2018

Researchers have confirmed that when a woman’s asthma medication is optimally during pregnancy, the rate of asthma in her offspring is nearly halved.

Asthma researchers' virus and allergy breakthrough

January 21, 2013

Paediatric and respiratory researchers from the University of Newcastle, along with national and international collaborators, are a step closer to identifying the source of serious virus-and allergen-induced asthma attacks after detecting important molecu

Professor Joerg Mattes

Position

Chair - Paediatrics & Child Health
Experimental&Translational Respiratory Medicine Group
School of Medicine and Public Health
Faculty of Health and Medicine

Focus area

Immunology and Microbiology

Contact Details

Email joerg.mattes@newcastle.edu.au
Phone (02) 40420209 (02) 49213656
Fax (02) 49855277 (02) 40420023

Office

Room 2411
Building HMRI
Location Level 2 East, HMRI, Lot 1 Kookaburra Circuit, New Lambton Heights, NSW 2305, Australia

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