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Dr Katie Baines

Post-Doctoral Research Fellow

School of Medicine and Public Health

Untangling the web of asthma

Research Fellow Dr Katie Baines is identifying biomarkers and targeting neutrophil extracellular traps with the aim of alleviating severe asthma.

“I work in biomarkers and mechanisms of neutrophilic asthma,” Katie says.

Her research has led to a number of important contributions to the knowledge base particularly the role of neutrophils and gene expression in asthma and chronic obstructive pulmonary disease (COPD).

A major project looking at neutrophilic extracellular traps is about to begin.

Katie is also developing a panel of genes to diagnose and medicate for difference types of asthma, as symptoms can be very similar although caused by different underlying mechanisms.

“We are doing a lot of work to further the six gene biomarkers panel, which show the type of inflammation, obviously with the aim of creating a diagnostic tool,” Katie notes.

“In respiratory research I can explore lab based genetic aspects, but also have access to clinical samples and work on human research. I feel I can have a direct impact on patients by helping improve their health.”

Inflammation and asthma

Australia has one of the highest rates of asthma in the world, and traditional treatments are not universally efficacious.

‘There are different types of asthma and they are driven by different types of inflammation,’ Katie states.

The most common form of asthma is caused by eosinophils, white blood cells created by the immune system to address allergies.

“But at least half of people with asthma do not have these cells in their airways,” Katie says.

Instead, neutrophils, another type of white blood cell created by the immune system, are released into the blood, and find their way to the lungs. When eosinophils or neutrophils become over active or accumulate, they create inflammation in the very area they are trying to protect.

Eosinophilic asthma responds to traditional asthma treatments such as short-acting β2 agonists relievers, and corticosteroid preventers.

Unfortunately, neutrophilic asthma is less responsive to these medications.

“So currently, a patient needs higher and higher doses although it is not working as well as it should.”

“We want to change that.”

Neutrophil extracellular traps

Katie believes that studying neutrophils is the key to better treatment for neutrophilic asthma.

“There are no optimised treatments for neutrophilic asthmatics because we don't know much about the mechanism of neutrophilic inflammation.”

Neutrophils release a meshwork of fibers in a web-like trap called neutrophil extracellular traps (NETs), which are made of the cells’ DNA and other proteins that fight infection.

“These webs are a good thing, they are catching the bugs and doing their job,” Katie says.

“But when they get uncontrolled or they accumulate too much, they can be so inflammatory, and make your mucus really thick and sticky. That would stop you clearing your infection.”

Accordingly, Katie is currently working on a theory that targeting NETs could reduce inflammation in severe asthma.

Pulmozyme, a medication currently used to reduce viscosity of mucus in cystic fibrosis sufferers, will be trialed by Katie to test its ability to breakdown the DNA backbone of NETs.

The magic six biomarkers

Originally a molecular biologist, Katie has worked solidly on identifying gene expression biomarkers. By measuring the activity of a panel of six genes, she can pinpoint what type of inflammation a patient has.

“If for example you had eosinophilic inflammation, three of the genes would be high, and the other ones would be low. But if you have neutrophilic inflammation, the other three will be high. And if you have both, well all genes will be high.”

“By having this panel, we are hoping to be able to say, okay, you've got this type of inflammation, and this treatment will work best for you,” Katie says.

“So we’re making treatment more personalised, and thereby more effective.”

Early Success

Katie studied Biomedical Science at the University of Newcastle, as she always had an interest in how the body works and how it is affected in disease.

As an early career researcher, the significance of Katie’s work has been quickly recognised. Throughout her PhD, she received support from The Asthma Foundation of NSW and The Cooperative Research Centre (CRC) for Asthma and Airways.

Since graduating, she has received research fellowships from the Thoracic Society of Australia and New Zealand, National Asthma Council, Xstrata Coal as well as the Australian Lung Foundation.

Katie is co-supervising eight students and is committed to providing a supportive environment for students to grow and learn the skills that will allow them to be successful in their independent research in the future.

Collaborating with others in the field is a priority, and thus Katie is a principal researcher at UON’s Priority Research Centre for Healthy Lungs. Katie also leads a molecular mechanisms group within VIVA (Viruses, Infections/Immunity, Vaccines and Asthma) at HMRI.

Untangling the web of asthma

Katie is a laboratory based researcher with expertise in many methods, including using molecular techniques to address respiratory disease.

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Career Summary

Biography

Dr Baines is a post doctoral researcher in the Department of Respiratory and Sleep Medicine, Hunter Medical Research Institute, and the Priority Research Centre for Asthma and Respiratory Disease. Her second 3 year post-doctoral fellowship commenced in January 2012 through The University of Newcastle, and prior to this she received a research fellowship through (2008-11) funded through Xstrata Coal and HMRI. As an early career post doctoral researcher; Dr Baines manages a semi independent molecular mechanisms group within Professor Peter Gibson’s laboratory. Dr Baines interest in respiratory medicine began when she commenced PhD studies in late 2003 (awarded in 2008), on molecular mechanisms involved in the pathogenesis of noneosinophilic asthma, particularly involving neutrophils. Throughout her PhD she was supported with scholarships from The Asthma Foundation of NSW and the Asthma CRC. Dr Baines is committed to furthering a full-time career in medical research. Her research interests surround the role of gene-environment interactions in the development and pathogenesis of respiratory diseases including asthma and COPD. Dr Baines research uses high throughput genomics technologies to understand more about molecular mechanisms, particularly phenotype definition, biomarker identification and the relationship of phenotypes to clinical outcomes and treatment responses. She is also interested in how respiratory disease phenotypes evolve over time, with regard to the impact of medication use such as inhaled corticosteroids and macrolides, and environmental exposures such as diet and microbial infection. Dr Baines research has led to a number of important contributions to the knowledge base particularly the role of neutrophils and gene expression in asthma and COPD. She has shown that airway neutrophils have an impaired innate immune response in asthma; however blood neutrophils are activated in the neutrophilic phenotype of asthma which is associated with systemic inflammation, a key feature of this phenotype. Dr Baines has defined transcriptional phenotypes of asthma using gene expression profiling of induced sputum and blood, proving the existence of phenotypes as well as the involvement of specific pathways (IL1 and TNF) in the pathogenesis of neutrophilic airway inflammation. Dr Baines has recently identified novel immune genes that are associated with rhinovirus infection of airway epithelial cells in COPD. Since 2009 Dr Baines has published >15 journal articles in highly ranked journals (Thorax, ERJ, JACI), that have been cited 138 times at present. She also has 2 book chapters, 1 Australian Provisional Patent and >38 conference abstracts. Dr Baines has obtained several awards, including the New and Emerging Researcher Awards in 2011 from the Australian Lung Foundation and the Thoracic Society of Australia and New Zealand. She has been awarded 7 competitive travel grant awards, including the esteemed Janet Elder Travel Grant in 2011 and the HMRI Pulse Education Prize in 2010. Dr Baines currently co-supervises 3 PhD students, and was primary supervisor to an honours student who received Class 1 honours in 2012. She is committed to providing a supportive environment for students to grow and learn the skills that will allow them to be successful in their independent research in the future.

Research Expertise

Katie is a laboratory based researcher with expertise in many laboratory methods, including using molecular techniques to understand more about the pathogenesis of respiratory diseases, including asthma and chronic obstructive pulmonary disease (COPD). She has particularl interest in using transcriptomics to understand how environmental influences in predisposed individuals can lead to the development of respiratory disease and different phenotypes of disease. She is also particularly interested in the role of inflammatory cells especially neutrophils in asthma and COPD, and the effects of environmental exposures including medications, diet and infection.

Collaborations
Dr Baines is involved in several successful collaborations, both locally and nationally. 1. Prof Anne Chang, Menzies School of Health and University of Queensland: A new multi-site study investigating airway and systemic markers and mechanisms of Protracted Bacterial Bronchitis in children. Subject of an NHMRC funded grant 2013-2016 2. Dr Manuel Ferreira, University of Queensland: Characterisation of the asthma transcriptome using RNA-seq. Subject of a UQ Collaborative Seed Funding Grant 2012. 3. Dr Brian Oliver and Prof Dominik Hartl, Woolcock Research Institute, University of Sydney, and University of Tubingen, Germany. Neutrophil responses to rhinovirus infection in asthma. Subject of a pending NHMRC grant for 2014. Local collaborations: 1. Prof Peter Gibson and Dr Jodie Simpson: Markers and Mechanisms of severe asthma inflammatory phenotypes. Subject of a NHMRC grant 2013-2015. 2. Dr Vanessa McDonald and Prof Peter Gibson: Phenotype based management of severe asthma. Funded by HMRI and John Hunter Hospital Charitable Trust 2012. 2. Dr Lisa Wood: Effects of diet, including antioxidant withdrawal and fatty acids on gene expression in asthma. 3. A/Prof Peter Wark: Rhinovirus infection and changes in gene expression in primary bronchial epithelial cells in COPD and asthma.

Qualifications

  • PhD, University of Newcastle
  • Bachelor of Biomedical Sciences, University of Newcastle
  • Bachelor of Biomedical Sciences (Hons), University of Newcastle

Keywords

  • Asthma
  • COPD
  • Epigenetics
  • Gene Expression
  • Inflammation
  • Innate Immunity
  • Neutrophils

Fields of Research

Code Description Percentage
110203 Respiratory Diseases 100

Professional Experience

UON Appointment

Title Organisation / Department
Post-Doctoral Research Fellow University of Newcastle
School of Medicine and Public Health
Australia

Academic appointment

Dates Title Organisation / Department
1/01/2015 -  Fellow UON

UoN Research Fellowship

University of Newcastle
School of Medicine and Public Health
Australia
1/01/2012 -  Post Doctoral Research Fellow University of Newcastle
School of Medicine and Public Health
Australia
1/05/2008 - 1/12/2011 Post Doctoral Fellow University of Newcastle
School of Medicine and Public Health
Australia
1/04/2008 - 1/04/2011 Fellow

Hunter Medical Research Institute:- Project Grant

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
2013 Baines KJ, Simpson JL, Gibson PG, 'Biology of Neutrophils', Middleton's Allergy: Principles and Practice: Eighth Edition 280-191 (2013)
DOI 10.1016/B978-0-323-08593-9.00018-8
Citations Scopus - 1
Co-authors Peter Gibson, Jodie Simpson
2009 Simpson JL, Baines KJ, Gibson PG, 'Biology of neutrophils', Middleton's Allergy: Principles & Practice, Mosby, Philadelphia, Pennsylvania 283-294 (2009) [B1]
Co-authors Peter Gibson, Jodie Simpson

Journal article (54 outputs)

Year Citation Altmetrics Link
2017 Kim RY, Pinkerton JW, Essilfie AT, Robertson AA, Baines KJ, Brown AC, et al., 'Role for NLRP3 Inflammasome-mediated, IL-1ß-dependent Responses in Severe, Steroid-resistant Asthma.', Am J Respir Crit Care Med, (2017)
DOI 10.1164/rccm.201609-1830OC
Co-authors Darryl Knight, Jay Horvat, Philip Hansbro, Jodie Simpson, Lisa Wood, Peter Gibson, Nicole Hansbro, Malcolm Starkey, Peter Wark
2017 Baines KJ, Fu JJ, McDonald VM, Gibson PG, 'Airway gene expression of IL-1 pathway mediators predicts exacerbation risk in obstructive airway disease', International Journal of COPD, 12 541-550 (2017)

© 2017 Baines et al.Background: Exacerbations of asthma and COPD are a major cause of morbidity and mortality and are responsible for significant health care costs. This study fu... [more]

© 2017 Baines et al.Background: Exacerbations of asthma and COPD are a major cause of morbidity and mortality and are responsible for significant health care costs. This study further investigates interleukin (IL)-1 pathway activation and its relationship with exacerbations of asthma and COPD. Methods: In this prospective cohort study, 95 participants with stable asthma (n=35) or COPD (n=60) were recruited and exacerbations recorded over the following 12 months. Gene expressions of IL-1 pathway biomarkers, including the IL-1 receptors (IL1R1, IL1R2, and IL1RN), and signaling molecules (IRAK2, IRAK3, and PELI1), were measured in sputum using real-time quantitative polymerase chain reaction. Mediators were compared between the frequent (2 exacerbations in the 12 months) and infrequent exacerbators, and the predictive relationships investigated using receiver operating characteristic curves and area under the curve (AUC) values. Results: Of the 95 participants, 89 completed the exacerbation follow-up, where 30 participants (n=22 COPD, n=8 asthma) had two or more exacerbations. At the baseline visit, expressions of IRAK2, IRAK3, PELI1, and IL1R1 were elevated in participants with frequent exacerbations of both asthma and COPD combined and separately. In the combined population, sputum gene expression of IRAK3 (AUC=75.4%; P,0.001) was the best predictor of future frequent exacerbations, followed by IL1R1 (AUC=72.8%; P,0.001), PELI1 (AUC=71.2%; P,0.001), and IRAK2 (AUC=68.6; P=0.004). High IL-1 pathway gene expression was associated with frequent prior year exacerbations and correlated with the number and severity of exacerbations. Conclusion: The upregulation of IL-1 pathway mediators is associated with frequent exacerbations of obstructive airway disease. Further studies should investigate these mediators as both potential diagnostic biomarkers predicting at-risk patients and novel treatment targets.

DOI 10.2147/COPD.S119443
Co-authors Vanessa Mcdonald, Peter Gibson
2017 Williams EJ, Baines KJ, Berthon BS, Wood LG, 'Effects of an encapsulated fruit and vegetable juice concentrate on obesity-induced systemic inflammation: A randomised controlled trial', Nutrients, 9 (2017)

© 2017 by the authors; licensee MDPI, Basel, Switzerland.Phytochemicals from fruit and vegetables reduce systemic inflammation. This study examined the effects of an encapsulated... [more]

© 2017 by the authors; licensee MDPI, Basel, Switzerland.Phytochemicals from fruit and vegetables reduce systemic inflammation. This study examined the effects of an encapsulated fruit and vegetable (F&V) juice concentrate on systemic inflammation and other risk factors for chronic disease in overweight and obese adults. A double-blinded, parallel, randomized placebo-controlled trial was conducted in 56 adults aged =40 years with a body mass index (BMI) =28 kg/m2. Before and after eight weeks daily treatment with six capsules of F&V juice concentrate or placebo, peripheral blood gene expression (microarray, quantitative polymerase chain reaction (qPCR)), plasma tumour necrosis factor (TNF)a (enzyme-linked immunosorbent assay (ELISA)), body composition (Dual-energy X-ray absorptiometry (DEXA)) and lipid profiles were assessed. Following consumption of juice concentrate, total cholesterol, low-density lipoprotein (LDL) cholesterol and plasma TNFa decreased and total lean mass increased, while there was no change in the placebo group. In subjects with high systemic inflammation at baseline (serum C-reactive protein (CRP) =3.0 mg/mL) who were supplemented with the F&V juice concentrate (n = 16), these effects were greater, with decreased total cholesterol, LDL cholesterol and plasma TNFa and increased total lean mass; plasma CRP was unchanged by the F&V juice concentrate following both analyses. The expression of several genes involved in lipogenesis, the nuclear factor-¿B (NF-¿B) and 5' adenosine monophosphate-activated protein kinase (AMPK) signalling pathways was altered, including phosphomevalonate kinase (PMVK), zinc finger AN1-type containing 5 (ZFAND5) and calcium binding protein 39 (CAB39), respectively. Therefore, F&V juice concentrate improves the metabolic profile, by reducing systemic inflammation and blood lipid profiles and, thus, may be useful in reducing the risk of obesity-induced chronic disease.

DOI 10.3390/nu9020116
Co-authors Lisa Wood
2017 Baines KJ, Fu J-J, McDonald VM, Gibson PG, 'Airway gene expression of IL-1 pathway mediators predicts exacerbation risk in obstructive airway disease', INTERNATIONAL JOURNAL OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE, 12 541-550 (2017)
DOI 10.2147/COPD.S119443
Co-authors Peter Gibson, Vanessa Mcdonald
2017 Halnes I, Baines KJ, Berthon BS, MacDonald-Wicks LK, Gibson PG, Wood LG, 'Soluble Fibre Meal Challenge Reduces Airway Inflammation and Expression of GPR43 and GPR41 in Asthma.', Nutrients, 9 (2017)
DOI 10.3390/nu9010057
Co-authors Lisa Wood, Lesley Wicks, Peter Gibson
2017 Hsu A, Dua K, Starkey MR, Haw TJ, Nair PM, Nichol K, et al., 'MicroRNA-125a and -b inhibit A20 and MAVS to promote inflammation and impair antiviral response in COPD', JOURNAL OF CLINICAL INVESTIGATION (JCI) Insight, (2017)
DOI 10.1172/jci.insight.90443
Co-authors Philip Hansbro, Alan Hsu, Malcolm Starkey, Peter Wark, Paul Foster
2016 Li Q, Baines KJ, Gibson PG, Wood LG, 'Changes in expression of genes regulating airway inflammation following a high-fat mixed meal in asthmatics', Nutrients, 8 (2016) [C1]

© 2016 by the authors; licensee MDPI, Basel, Switzerland.Consumption of a high fat meal can increase neutrophilic airway inflammation in asthma subjects. This study investigates ... [more]

© 2016 by the authors; licensee MDPI, Basel, Switzerland.Consumption of a high fat meal can increase neutrophilic airway inflammation in asthma subjects. This study investigates the molecular mechanisms driving airway neutrophilia following a high fat meal in asthmatics. Subjects with asthma (n = 11) and healthy controls (n = 8) consumed a high-fat/energy meal, containing total energy (TE) of 3846 kJ and 48 g of total fat (20.5 g saturated). Sputum was induced at 0 and 4 h, and gene expression was examined by microarray and quantitative real-time PCR (qPCR). Following the high fat dietary challenge, 168 entities were significantly differentially expressed greater than >1.5 fold in subjects with asthma, whereas, in healthy controls, only 14 entities were differentially expressed. Of the 168 genes that were changed in asthma, several biological processes were overrepresented, with 25 genes involved in "immune system processes". qPCR confirmed that S100P, S100A16, MAL and MUC1 were significantly increased in the asthma group post-meal. We also observed a strong correlation and a moderate correlation between the change in NLRP12 and S100A16 gene expression at 4 h compared to baseline, and the change in total and saturated non-esterified plasma fatty acid levels at 2 h compared to baseline. In summary, our data identifies differences in inflammatory gene expression that may contribute to increased airway neutrophilia following a high fat meal in subjects with asthma and may provide useful therapeutic targets for immunomodulation. This may be particularly relevant to obese asthmatics, who are habitually consuming diets with a high fat content.

DOI 10.3390/nu8010030
Citations Scopus - 1Web of Science - 1
Co-authors Lisa Wood, Peter Gibson
2016 Wang G, Baines KJ, Fu JJ, Wood LG, Simpson JL, McDonald VM, et al., 'Sputum mast cell subtypes relate to eosinophilia and corticosteroid response in asthma', European Respiratory Journal, 47 1123-1133 (2016) [C1]

Copyright © ERS 2016.Mast cells are a resident inflammatory cell of the airways, involved in both the innate and adaptive immune response. The relationship between mast cells and... [more]

Copyright © ERS 2016.Mast cells are a resident inflammatory cell of the airways, involved in both the innate and adaptive immune response. The relationship between mast cells and inflammatory phenotypes and treatment response of asthma is not clear. Clinical characteristics of subjects with stable asthma (n=55), inflammatory cell counts and gene expression microarrays in induced sputum were analysed. Sputum mast cell subtypes were determined by molecular phenotyping based on expression of mast cell biomarkers (tryptase (TPSAB1), chymase (CMA1) and carboxypeptidase A3 (CPA3)). Effects of mast cell subtypes on steroid response were observed in a prospective cohort study (n=50). MCT (n=18) and MCT/CPA3 (mRNA expression of TPSAB1 and CPA3; n=29) subtypes were identified, as well as a group without mast cell gene expression (n=8). The MCT/CPA3 subtype had elevated exhaled nitric oxide fraction, sputum eosinophils, bronchial sensitivity and reactivity, and poorer asthma control. This was accompanied by upregulation of 13 genes. Multivariable logistic regression identified CPA3 (OR 1.21, p=0.004) rather than TPSAB1 (OR 0.92, p=0.502) as a determinant of eosinophilic asthma. The MCT/CPA3 subtype had a better clinical response and reduced signature gene expression with corticosteroid treatment. Sputum mast cell subtypes of asthma can be defined by a molecular phenotyping approach. The MCT/CPA3 subtype demonstrated increased bronchial sensitivity and reactivity, and signature gene expression, which was associated with airway eosinophilia and greater corticosteroid responsiveness.

DOI 10.1183/13993003.01098-2015
Citations Scopus - 5Web of Science - 5
Co-authors Jodie Simpson, Vanessa Mcdonald, Lisa Wood, Peter Gibson
2016 Tang FSM, Van Ly D, Spann K, Reading PC, Burgess JK, Hartl D, et al., 'Differential neutrophil activation in viral infections: Enhanced TLR-7/8-mediated CXCL8 release in asthma', Respirology, 21 172-179 (2016) [C1]

© 2015 The Authors. Respirology published by Wiley Publishing Asia Pty Ltd on behalf of Asian Pacific Society of Respirology.Background and objective Respiratory viral infections... [more]

© 2015 The Authors. Respirology published by Wiley Publishing Asia Pty Ltd on behalf of Asian Pacific Society of Respirology.Background and objective Respiratory viral infections are a major cause of asthma exacerbations. Neutrophils accumulate in the airways and the mechanisms that link neutrophilic inflammation, viral infections and exacerbations are unclear. This study aims to investigate anti-viral responses in neutrophils from patients with and without asthma and to investigate if neutrophils can be directly activated by respiratory viruses. Methods Neutrophils from peripheral blood from asthmatic and non-asthmatic individuals were isolated and stimulated with lipopolysaccharide (LPS) (1 µg/mL), f-met-leu-phe (fMLP) (100 nM), imiquimod (3 µg/mL), R848 (1.5 µg/mL), poly I:C (10 µg/mL), RV16 (multiplicity of infection (MOI)1), respiratory syncytial virus (RSV) (MOI1) or influenza virus (MOI1). Cell-free supernatants were collected after 1 h of neutrophil elastase (NE) and matrix metalloproteinase (MMP)-9 release, or after 24 h for CXCL8 release. Results LPS, fMLP, imiquimod and R848 stimulated the release of CXCL8, NE and MMP-9 whereas poly I:C selectively induced CXCL8 release only. R848-induced CXCL8 release was enhanced in neutrophils from asthmatics compared with non-asthmatic cells (P < 0.01). RSV triggered the release of CXCL8 and NE from neutrophils, whereas RV16 or influenza had no effect. Conclusion Neutrophils release CXCL8, NE and MMP-9 in response to viral surrogates with R848-induced CXCL8 release being specifically enhanced in asthmatic neutrophils. Toll-like receptor (TLR7/8) dysregulation may play a role in neutrophilic inflammation in viral-induced exacerbations. We aimed to investigate and compare neutrophil responses to bacterial compounds and viral mimetics as well as compare responses between people with and without asthma. We also investigated neutrophil responses to live respiratory viruses. Here we provide a novel comprehensive comparison showing differential and specific activation in innate immune cells. See Editorial, page 10

DOI 10.1111/resp.12657
Citations Scopus - 8Web of Science - 8
2016 Simpson JL, Baines KJ, Horvat JC, Essilfie AT, Brown AC, Tooze M, et al., 'COPD is characterized by increased detection of Haemophilus influenzae, Streptococcus pneumoniae and a deficiency of Bacillus species', Respirology, 21 697-704 (2016) [C1]

© 2016 Asian Pacific Society of Respirology.Background and objective Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow limitation and inflammat... [more]

© 2016 Asian Pacific Society of Respirology.Background and objective Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow limitation and inflammation. Airway bacterial colonization is increased in COPD; however, the role of potentially pathogenic and non-pathogenic bacteria in the pathogenesis of disease is unclear. This study characterized the presence of bacteria in a well-characterized cohort of adults with COPD and healthy controls. Methods Adults with COPD (n = 70) and healthy controls (n = 51) underwent clinical assessment and sputum induction. Sputum was dispersed, and total and differential cell counts were performed. Bacteria were cultured, identified and enumerated. Supernatants were assessed for neutrophil elastase (NE) and IL-1ß. Common respiratory pathogens were also determined using real-time PCR. Results Participants with COPD had a typical neutrophilic inflammatory profile. The total load of bacteria was increased in COPD and was associated with poorer respiratory health status, as measured by the St George's Respiratory Questionnaire (Spearman's r = 0.336, P = 0.013). Significantly lower levels of culturable Bacillus species were identified compared with healthy controls. PCR analyses revealed increased rates of detection of potentially pathogenic bacteria with Haemophilus influenzae detection associated with higher sputum levels of NE and IL-1ß, while Streptococcus pneumoniae was more common in male ex-smokers with emphysema and a deficit in diffusion capacity. Conclusion Non-pathogenic and pathogenic bacteria were altered in the sputum of patients with COPD. These observations highlight the potential to identify treatment and management strategies that both target specific bacterial pathogens and restore the microbial balance, which may lead to reductions in inflammation and subsequent improvements in lung health.

DOI 10.1111/resp.12734
Citations Scopus - 5Web of Science - 6
Co-authors Vanessa Mcdonald, Jodie Simpson, Philip Hansbro, Peter Gibson, Jay Horvat
2016 Sverrild A, Bergqvist A, Baines KJ, Porsbjerg C, Andersson CK, Thomsen SF, et al., 'Airway responsiveness to mannitol in asthma is associated with chymase-positive mast cells and eosinophilic airway inflammation', Clinical and Experimental Allergy, 46 288-297 (2016) [C1]

© 2016 John Wiley & Sons Ltd.Background: Airway hyperresponsiveness (AHR) to inhaled mannitol is associated with indirect markers of mast cell activation and eosinophilic airway ... [more]

© 2016 John Wiley & Sons Ltd.Background: Airway hyperresponsiveness (AHR) to inhaled mannitol is associated with indirect markers of mast cell activation and eosinophilic airway inflammation. It is unknown how AHR to mannitol relates to mast cell phenotype, mast cell function and measures of eosinophilic inflammation in airway tissue. We compared the number and phenotype of mast cells, mRNA expression of mast cell-associated genes and number of eosinophils in airway tissue of subjects with asthma and healthy controls in relation to AHR to mannitol. Methods: Airway hyperresponsiveness to inhaled mannitol was measured in 23 non-smoking, corticosteroid-free asthmatic individuals and 10 healthy controls. Mast cells and eosinophils were identified in mucosal biopsies from all participants. Mast cells were divided into phenotypes based on the presence of chymase. mRNA expression of mast cell-associated genes was measured by real-time PCR. Results: The proportion of submucosal MCTC was higher in asthmatic individuals with AHR to mannitol compared with asthmatic individuals without AHR (median: 40.3% vs. 18.7%, P=0.03). Increased submucosal MCTC numbers were associated with increased levels of mRNA for thymic stromal lymphopoietin (TSLP) and CPA3 in asthmatics. Reactivity to mannitol correlated significantly with eosinophils in submucosa (r(s): 0.56, P=0.01). Conclusion: Airway hyperresponsiveness to inhaled mannitol is associated with an altered submucosal mast cell profile in asthmatic individuals. This mast cell profile is associated with increased levels of TSLP and CPA3. The degree of AHR to mannitol is correlated with the degree of eosinophilic inflammation in the airway submucosa.

Citations Scopus - 4Web of Science - 4
Co-authors Peter Gibson
2016 Nguyen TH, Maltby S, Simpson JL, Eyers F, Baines KJ, Gibson PG, et al., 'TNF-a and macrophages are critical for respiratory syncytial virus-induced exacerbations in a mouse model of allergic airways disease', Journal of Immunology, 196 3547-3558 (2016) [C1]

Viral respiratory infections trigger severe exacerbations of asthma, worsen disease symptoms, and impair lung function. To investigate the mechanisms underlying viral exacerbation... [more]

Viral respiratory infections trigger severe exacerbations of asthma, worsen disease symptoms, and impair lung function. To investigate the mechanisms underlying viral exacerbation, we established a mouse model of respiratory syncytial virus (RSV)-induced exacerbation after allergen sensitization and challenge. RSV infection of OVA-sensitized/challenged BALB/c mice resulted in significantly increased airway hyperresponsiveness (AHR) and macrophage and neutrophil lung infiltration. Exacerbation was accompanied by increased levels of inflammatory cytokines (including TNF-a, MCP-1, and keratinocyte-derived protein chemokine [KC]) compared with uninfected OVA-treated mice or OVA-treated mice exposed to UV-inactivated RSV. Dexamethasone treatment completely inhibited all features of allergic disease, including AHR and eosinophil infiltration, in uninfected OVAsensitized/challenged mice. Conversely, dexamethasone treatment following RSV-induced exacerbation only partially suppressed AHR and failed to dampen macrophage and neutrophil infiltration or inflammatory cytokine production (TNF-a, MCP-1, and KC). This mimics clinical observations in patients with exacerbations, which is associated with increased neutrophils and often poorly responds to corticosteroid therapy. Interestingly, we also observed increased TNF-a levels in sputum samples from patients with neutrophilic asthma. Although RSV-induced exacerbation was resistant to steroid treatment, inhibition of TNF-a and MCP-1 function or depletion of macrophages suppressed features of disease, including AHR and macrophage and neutrophil infiltration. Our findings highlight critical roles for macrophages and inflammatory cytokines (including TNF-a and MCP-1) in viral-induced exacerbation of asthma and suggest examination of these pathways as novel therapeutic approaches for disease management.

DOI 10.4049/jimmunol.1502339
Citations Scopus - 2Web of Science - 2
Co-authors Peter Gibson, Ming Yang, Paul Foster, Steven Maltby, Jodie Simpson
2016 Wright TK, Gibson PG, Simpson JL, McDonald VM, Wood LG, Baines KJ, 'Neutrophil extracellular traps are associated with inflammation in chronic airway disease', Respirology, 21 467-475 (2016) [C1]

© 2016 Asian Pacific Society of Respirology.Background and objective Neutrophil extracellular traps (NETs) are web-like structures comprising DNA and antimicrobial proteins, expe... [more]

© 2016 Asian Pacific Society of Respirology.Background and objective Neutrophil extracellular traps (NETs) are web-like structures comprising DNA and antimicrobial proteins, expelled from neutrophils during NETosis. Persistence of NETs can be pro-inflammatory, yet their role in respiratory disease remains unclear. This study aimed to investigate the presence of NETs in sputum from patients with asthma and COPD, and the relationship of NETs with inflammatory phenotype and disease severity. Methods Induced sputum was collected from healthy controls, asthma and COPD patients. Extracellular DNA (eDNA) was quantified by PicoGreen. LL-37, a-defensins1-3, NE, IL-1ß and CXCL8 were quantified by ELISA. PAD4 and NLRP3 gene expression was performed using qPCR. NETs were imaged in sputum smears using immunofluorescence microscopy. Results Sputum eDNA and NET neutrophil antimicrobial proteins were significantly elevated in asthma and COPD compared with healthy controls. Levels of eDNA and NET components were significantly higher in neutrophilic versus non-neutrophilic asthma and COPD. NETs were clearly visualized in sputum smears. PAD4 mRNA was upregulated in neutrophilic COPD. The level of eDNA was higher in severe asthma. High eDNA levels were associated with heightened innate immune responses, including elevated CXCL8 and IL-1ß, and NLRP3 gene expression in both COPD and asthma. Antimicrobial proteins and eDNA were positively correlated with airway neutrophils, and negatively correlated with lung function and symptoms. Conclusion NETs are present in the airways of subjects with asthma and COPD. Accumulation of excessive NETs was associated with activation of innate immune responses contributing to disease pathogenesis in chronic airway disease.

DOI 10.1111/resp.12730
Citations Scopus - 9Web of Science - 7
Co-authors Jodie Simpson, Vanessa Mcdonald, Lisa Wood, Peter Gibson
2016 Tang FSM, Hansbro PM, Burgess JK, Ammit AJ, Baines KJ, Oliver BG, 'A novel immunomodulatory function of neutrophils on rhinovirus-Activated monocytes in vitro', Thorax, 71 1039-1049 (2016) [C1]

© 2016 Published by the BMJ Publishing Group Limited.Background Rhinovirus (RV) infections are the major precipitant of asthma exacerbations. While neutrophilic lung inflammation... [more]

© 2016 Published by the BMJ Publishing Group Limited.Background Rhinovirus (RV) infections are the major precipitant of asthma exacerbations. While neutrophilic lung inflammation occurs during such infections, its role remains unclear. Neutrophilic inflammation is associated with increased asthma severity and steroid refractory disease. Neutrophils are vital for controlling infections but also have immunomodulatory functions. Previously, we found that neutrophils respond to viral mimetics but not replication competent RV. We aimed to investigate if neutrophils are activated and/or modulate immune responses of monocytes during RV16 infection. Methods Primary human monocytes and autologous neutrophils were cocultured with or without RV16, in direct contact or separated by transwells. RV16-stimulated monocytes were also exposed to lysed neutrophils, neutrophil membrane components or soluble neutrophil intracellular components. Interleukin 6 (IL-6) and C-X-C motif (CXC)L8 mRNA and proteins were measured by quantitative PCR and ELISA at 24â ¿..hours. Results RV16 induced IL-6 and CXCL8 in monocytes, but not neutrophils. RV16-induced IL-6 and CXCL8 from monocytes was reduced in the presence of live neutrophils. Transwell separation abolished the inhibitory effects. Lysed neutrophils inhibited RV16-induced IL-6 and CXCL8 from monocytes. Neutrophil intracellular components alone effectively inhibited RV16-induced monocyte-derived IL-6 and CXCL8. Neutrophil intracellular components reduced RV16-induced IL-6 and CXCL8 mRNA in monocytes. Conclusions Cell contact between monocytes and neutrophils is required, and preformed neutrophil mediator(s) are likely to be involved in the suppression of cytokine mRNA and protein production. This study demonstrates a novel regulatory function of neutrophils on RV-Activated monocytes in vitro, challenging the paradigm that neutrophils are predominantly proinflammatory.

DOI 10.1136/thoraxjnl-2015-207781
Citations Scopus - 4Web of Science - 3
Co-authors Philip Hansbro
2016 Simpson JL, Daly J, Baines KJ, Yang IA, Upham JW, Reynolds PN, et al., 'Airway dysbiosis: Haemophilus influenza and Tropheryma in poorly controlled asthma', European Respiratory Journal, 47 792-800 (2016) [C1]

© ERS 2016.Asthma is a chronic inflammatory disorder of the airways where bacteria may act as protagonists of chronic inflammation. Little is known about the relation of airway i... [more]

© ERS 2016.Asthma is a chronic inflammatory disorder of the airways where bacteria may act as protagonists of chronic inflammation. Little is known about the relation of airway inflammation to the presence of specific bacterial taxa. We sought to describe the sputum microbiome in adults with poorly controlled asthma. DNA was extracted from induced sputum and microbial communities were profiled using 16S rRNA pyrosequencing. Bacterial species were characterised, and the relationship between microbial populations, asthma inflammatory subtypes and other covariates was explored. Real-time PCR was used to identify Tropheryma whipplei and Haemophilus influenzae in sputum. Adults with neutrophilic asthma had reduced bacterial diversity and species richness. Tropheryma was identified and confirmed with real-time PCR in 12 (40%) participants. Haemophilus occurred most often in a group of younger atopic males with an increased proportion of neutrophils. PCR confirmed the presence of H. influenzae in 35 (76%) participants with poorly controlled asthma. There are phenotype-specific alterations to the airway microbiome in asthma. Reduced bacterial diversity combined with a high prevalence of H. influenzae was observed in neutrophilic asthma, whereas eosinophilic asthma had abundant T. whipplei.

DOI 10.1183/13993003.00405-2015
Citations Scopus - 17Web of Science - 18
Co-authors Peter Gibson, Jodie Simpson
2016 Hodge S, Upham JW, Pizzutto S, Petsky HL, Yerkovich S, Baines KJ, et al., 'Is alveolar macrophage phagocytic dysfunction in children with protracted bacterial bronchitis a forerunner to bronchiectasis?', Chest, 149 508-515 (2016) [C1]

Copyright © 2016 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.Background: Children with recurrent protracted bacterial bronchitis (PBB) an... [more]

Copyright © 2016 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.Background: Children with recurrent protracted bacterial bronchitis (PBB) and bronchiectasis share common features, and PBB is likely a forerunner to bronchiectasis. Both diseases are associated with neutrophilic inflammation and frequent isolation of potentially pathogenic microorganisms, including nontypeable Haemophilus influenzae (NTHi), from the lower airway. Defective alveolar macrophage phagocytosis of apoptotic bronchial epithelial cells (efferocytosis), as found in other chronic lung diseases, may also contribute to tissue damage and neutrophil persistence. Thus, in children with bronchiectasis or PBB and in control subjects, we quantified the phagocytosis of airway apoptotic cells and NTHi by alveolar macrophages and related the phagocytic capacity to clinical and airway inflammation. Methods: Children with bronchiectasis (n = 55) or PBB (n = 13) and control subjects (n = 13) were recruited. Alveolar macrophage phagocytosis, efferocytosis, and expression of phagocytic scavenger receptors were assessed by flow cytometry. Bronchoalveolar lavage fluid interleukin (IL) 1ß was measured by enzyme-linked immunosorbent assay. Results: For children with PBB or bronchiectasis, macrophage phagocytic capacity was significantly lower than for control subjects (P=.003 and P<.001 for efferocytosis and P=.041 and P = .004 for phagocytosis of NTHi; PBB and bronchiectasis, respectively); median phagocytosis of NTHi for the groups was as follows: bronchiectasis, 13.7% (interquartile range [IQR], 11%-16%); PBB, 16% (IQR, 11%-16%); control subjects, 19.0% (IQR, 13%-21%); and median efferocytosis for the groups was as follows: bronchiectasis, 14.1% (IQR, 10%-16%); PBB, 16.2% (IQR, 14%-17%); control subjects, 18.1% (IQR, 16%-21%). Mannose receptor expression was significantly reduced in the bronchiectasis group (P = .019), and IL-1ß increased in both bronchiectasis and PBB groups vs control subjects. Conclusions: A reduced alveolar macrophage phagocytic host response to apoptotic cells or NTHi may contribute to neutrophilic inflammation and NTHi colonization in both PBB and bronchiectasis. Whether this mechanism also contributes to the progression of PBB to bronchiectasis remains unknown.

DOI 10.1016/j.chest.2015.10.066
Citations Scopus - 2Web of Science - 2
Co-authors Peter Gibson, Jodie Simpson
2016 Negewo NA, McDonald VM, Baines KJ, Wark PAB, Simpson JL, Jones PW, Gibson PG, 'Peripheral blood eosinophils: A surrogate marker for airway eosinophilia in stable COPD', International Journal of COPD, 11 1495-1504 (2016) [C1]

© 2016 Negewo et al.Introduction: Sputum eosinophilia occurs in approximately one-third of stable chronic obstructive pulmonary disease (COPD) patients and can predict exacerbati... [more]

© 2016 Negewo et al.Introduction: Sputum eosinophilia occurs in approximately one-third of stable chronic obstructive pulmonary disease (COPD) patients and can predict exacerbation risk and response to corticosteroid treatments. Sputum induction, however, requires expertise, may not always be successful, and does not provide point-of-care results. Easily applicable diagnostic markers that can predict sputum eosinophilia in stable COPD patients have the potential to progress COPD management. This study investigated the correlation and predictive relationship between peripheral blood and sputum eosinophils. It also examined the repeatability of blood eosinophil counts. Methods: Stable COPD patients (n=141) were classified as eosinophilic or noneosinophilic based on their sputum cell counts (=3%), and a cross-sectional analysis was conducted comparing their demographics, clinical characteristics, and blood cell counts. Receiver operating characteristic curve analysis was used to assess the predictive ability of blood eosinophils for sputum eosinophilia. Intraclass correlation coefficient was used to examine the repeatability of blood eosinophil counts. Results: Blood eosinophil counts were significantly higher in patients with sputum eosinophilia (n=45) compared to those without (0.3×109/L vs 0.15×109/L; P<0.0001). Blood eosinophils correlated with both the percentage (¿=0.535; P<0.0001) and number of sputum eosinophils (¿=0.473; P<0.0001). Absolute blood eosinophil count was predictive of sputum eosinophilia (area under the curve =0.76, 95% confidence interval [CI] =0.67¿0.84; P<0.0001). At a threshold of =0.3×109/L (specificity =76%, sensitivity =60%, and positive likelihood ratio =2.5), peripheral blood eosinophil counts enabled identification of the presence or absence of sputum eosinophilia in 71% of the cases. A threshold of =0.4×109/L had similar classifying ability but better specificity (91.7%) and higher positive likelihood ratio (3.7). In contrast, =0.2×109/L offered a better sensitivity (91.1%) for ruling out sputum eosinophilia. There was a good agreement between two measurements of blood eosinophil count over a median of 28 days (intraclass correlation coefficient =0.8; 95% CI =0.66¿0.88; P<0.0001). Conclusion: Peripheral blood eosinophil counts can help identify the presence or absence of sputum eosinophilia in stable COPD patients with a reasonable degree of accuracy.

DOI 10.2147/COPD.S100338
Citations Scopus - 4Web of Science - 1
Co-authors Peter Gibson, Peter Wark, Vanessa Mcdonald, Jodie Simpson
2016 Williams EJ, Baines KJ, Smart JM, Gibson PG, Wood LG, 'Rosuvastatin, lycopene and omega-3 fatty acids: A potential treatment for systemic inflammation in COPD; a pilot study', Journal of Nutrition and Intermediary Metabolism, 5 86-95 (2016) [C1]

© 2016 The AuthorsBackground/Aims Chronic Obstructive Pulmonary Disease (COPD) is characterized by airway inflammation, in which contributes to loss of lung function. Systemic in... [more]

© 2016 The AuthorsBackground/Aims Chronic Obstructive Pulmonary Disease (COPD) is characterized by airway inflammation, in which contributes to loss of lung function. Systemic inflammation is also a feature of COPD contributing to many associated co-morbidities. Statins, omega-3 fatty acids (docosahexanoic acid, DHA and eicosapentanoic acid, EPA) and lycopene have been shown to decrease systemic inflammation; however their combined effects have not been investigated. This study aims to identify changes in systemic and airway inflammation induced by statins alone or in combination with DHA, EPA and lycopene in COPD. Methods COPD patients (n¿=¿11) received rosuvastatin (20¿mg/day) for 4 weeks, then a combination of rosuvastatin (20¿mg/day), DHA and EPA (1.5¿g/day) and lycopene (45¿mg/day) for 8 weeks. Blood and sputum were collected and lung function measured by spirometry at baseline, week 4 and 12. Plasma fatty acids were measured using gas chromatography, while plasma carotenoids were analysed using high-performance liquid chromatography. Plasma CRP and IL-6 concentrations were measured using ELISA; and peripheral blood gene expression was measured using the nCounter¿ GX Human Inflammation Kit 2. Results Following the interventions, clinical characteristics and plasma IL-6 and CRP were unchanged. Sputum neutrophil proportion and absolute count was increased and macrophage proportion decreased by rosuvastatin (P¿=¿0.020 and P¿=¿0.015; respectively). Rosuvastatin increased LTB4R and decreased CXCL10 and AGER gene expression in white blood cells. The addition of lycopene and omega-3 fatty acids decreased LTB4R and increased CXCL10 to basal levels, whilst combined use of interventions increased ALOX15 blood gene expression. Conclusion This study shows that rosuvastatin, omega-3 fatty acids and lycopene have some anti-inflammatory effects systemically, but rosuvastatin may increase airway neutrophils, which would be undesirable in COPD patients, warranting further investigation.

DOI 10.1016/j.jnim.2016.04.006
Citations Scopus - 1
Co-authors Peter Gibson, Lisa Wood
2016 Porsbjerg C, Baines K, Gibson P, Bergqvist A, Erjefält JS, Sverrild A, Backer V, 'IL-33 is related to innate immune activation and sensitization to HDM in mild steroid-free asthma', Clinical and Experimental Allergy, 46 564-574 (2016) [C1]

© 2016 John Wiley & Sons Ltd.Summary: Background: IL-33 represents a potential link between the airway epithelium and induction of a Th2-type inflammatory response in asthma. How... [more]

© 2016 John Wiley & Sons Ltd.Summary: Background: IL-33 represents a potential link between the airway epithelium and induction of a Th2-type inflammatory response in asthma. However, the association with markers of eosinophilic airway inflammation has not previously been reported in patients with steroid-free asthma. Aim: To describe the relationship between airway IL-33 and markers of eosinophilic airway inflammation, as well potential triggers of IL-33, in mild, steroid-free asthma. Methods: IL-33 mRNA expression and IL-33 immunoreactivity were measured in bronchial biopsies from patients with asthma untreated with inhaled steroids and healthy individuals. Furthermore, fractional exhaled nitric oxide (FeNO) and eosinophils in sputum and BAL were measured, as well as airway hyperresponsiveness to mannitol and methacholine. Epithelial integrity was assessed by computerized image analysis on haematoxylin-stained sections, and TLR mRNA expression by PCR. Results: A total of 23 patients with asthma and 10 healthy individuals were examined (age: 24 years (20-40); females: 53%). The level of IL-33 mRNA expression was significantly higher in patients with asthma compared to healthy individuals (Median (IQR) 1.12 (0.78) vs. 0.86, P = 0.04). There was a positive correlation between IL-33 mRNA expression and the level of FeNO (r = 0.56, P = 0.01), whereas there was no association with airway or blood eosinophils. IL-33 expression was unrelated to loss of epithelial integrity, but correlated with an increased expression of TLR2 and TLR4 (TLR2: = 0.47, P = 0.04; TLR4: 0.68, P < 0.001), as well allergy to house dust mites (HDMs). Conclusion: In mild untreated asthma, the expression of IL-33 mRNA in bronchial mucosa is related to innate immune activation and allergic sensitization to HDM, rather than epithelial damage, and correlates with FeNO. These findings suggest that in mild allergic asthma, IL-33 may represent a link between innate immune activation and FeNO production.

DOI 10.1111/cea.12702
Citations Scopus - 2Web of Science - 1
Co-authors Peter Gibson
2015 Tang FSM, Foxley GJ, Gibson PG, Burgess JK, Baines KJ, Oliver BG, 'Altered Innate Immune Responses in Neutrophils from Patients with Well- and Suboptimally Controlled Asthma', Mediators of Inflammation, 2015 1-11 (2015) [C1]
DOI 10.1155/2015/219374
Citations Scopus - 1Web of Science - 1
Co-authors Peter Gibson
2015 Scott HA, Latham JR, Callister R, Pretto JJ, Baines K, Saltos N, et al., 'Acute exercise is associated with reduced exhaled nitric oxide in physically inactive adults with asthma', Annals of Allergy, Asthma and Immunology, 114 470-479 (2015) [C1]

© 2015 American College of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.Background Although exercise has multiple health benefits, relatively litt... [more]

© 2015 American College of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.Background Although exercise has multiple health benefits, relatively little attention has been paid to its potential therapeutic effects in those with asthma. Objective To examine the effects of acute exercise on inflammation in physically inactive and active adults with asthma. Methods Fourteen adults with asthma (n = 6 physically inactive, n = 8 physically active) completed (1) 30 minutes of moderate-intensity exercise on a treadmill and (2) 30 minutes of rest in random order, with 4 weeks between sessions. Exhaled nitric oxide (eNO) was measured before and after the intervention (0, 0.5, 1, 2, 4, and 24 hours). Blood inflammatory mediators were measured before and after the intervention (0, 2, and 24 hours). Results Physically inactive participants had a significant decrease in eNO 4 hours after exercise (-4.8 ppb, -6.4 to -0.5 ppb, P =.028), which was not observed in physically active participants (P =.362). Interluekin-1 receptor antagonist increased in the physically inactive group 2 hours after exercise, with this increase strongly correlated with the decrease in eNO at 4 hours (R = -0.685, P =.007) and 24 hours (R = -0.659, P =.014) after exercise. Interleukin-6 was increased significantly 2 hours after exercise in physically inactive participants. Blood neutrophils and nuclear factor erythroid 2-like 2 gene expression were increased 2 hours after exercise in the overall cohort. Conclusion This study demonstrates that acute moderate-intensity exercise is associated with decreased eNO in physically inactive adults with asthma and suggests that interluekin-1 receptor antagonist could have a role in mediating this effect. The attenuated response in physically active participants might be due to the sustained anti-inflammatory effects of exercise training. Future studies should investigate the impact of exercise intensity and exercise training on airway inflammation in those with asthma.

DOI 10.1016/j.anai.2015.04.002
Citations Scopus - 4Web of Science - 4
Co-authors Hayley Scott, Lisa Wood, Robin Callister
2015 Baines KJ, Backer V, Gibson PG, Powell H, Porsbjerg CM, 'Investigating the effects of arctic dietary intake on lung health', European Journal of Clinical Nutrition, 69 1262-1266 (2015) [C1]

© 2015 Macmillan Publishers Limited.Background/Objective:Preservation of lung health requires understanding the modifiable risk factors of airflow limitation. This study investig... [more]

© 2015 Macmillan Publishers Limited.Background/Objective:Preservation of lung health requires understanding the modifiable risk factors of airflow limitation. This study investigates the association between diet and lung function in a population of Greenland Inuit residing in the Arctic (Greenland) or Western Europe (Denmark).Subjects/Methods:Two unselected Inuit populations were recruited, one living in Greenland (Urban (Nuuk) n=358; Rural (Uummannaq) n=207) and the other in Denmark (n=539). Lung function was measured using spirometry and diet by a food frequency questionnaire. Factors associated with airflow limitation were assessed using multiple linear regression models.Results:The dietary composition differed significantly in the two regions, with higher whale, seal and wild meat intake and lower fruit and vegetable intake in the Arctic regions compared with Denmark. Consumption of vegetables (P=0.004) and whale and/or seal (P<0.0001) was significantly and positively associated with FEV 1, as well as with FVC (vegetables: P=0.001, whale and/or seal: P=0.002). Regular fruit intake was included in the statistical models; however, it did not reach statistical significance (FEV 1: P=0.053; FVC: P=0.055).Conclusions:High dietary intake of vegetables as well as intake of arctic marine mammals had independent positive associations with lung function in this cohort of Greenlandic Inuit. These findings suggest an additive role of dietary intake of antioxidants and unsaturated fatty acids in lung health, which warrants prospective evaluation.

DOI 10.1038/ejcn.2015.85
Citations Scopus - 1Web of Science - 2
Co-authors Peter Gibson
2015 Fu J-J, McDonald VM, Baines KJ, Gibson PG, 'Airway IL-1 beta and Systemic Inflammation as Predictors of Future Exacerbation Risk in Asthma and COPD', CHEST, 148 618-629 (2015) [C1]
DOI 10.1378/chest.14-2337
Citations Scopus - 19Web of Science - 18
Co-authors Peter Gibson, Vanessa Mcdonald
2015 Hodge G, Upham JW, Chang AB, Baines KJ, Yerkovich ST, Pizzutto SJ, Hodge S, 'Increased Peripheral Blood Pro-Inflammatory/Cytotoxic Lymphocytes in Children with Bronchiectasis', PLOS ONE, 10 (2015) [C1]
DOI 10.1371/journal.pone.0133695
Citations Scopus - 1Web of Science - 1
2015 Bowden NA, Beveridge NJ, Ashton KA, Baines KJ, Scott RJ, 'Understanding xeroderma pigmentosum complementation groups using gene expression profiling after UV-light exposure', International Journal of Molecular Sciences, 16 15985-15996 (2015) [C1]

© 2015 by the authors; licensee MDPI, Basel, Switzerland.Children with the recessive genetic disorder Xeroderma Pigmentosum (XP) have extreme sensitivity to UV-light, a 10,000-fo... [more]

© 2015 by the authors; licensee MDPI, Basel, Switzerland.Children with the recessive genetic disorder Xeroderma Pigmentosum (XP) have extreme sensitivity to UV-light, a 10,000-fold increase in skin cancers from age 2 and rarely live beyond 30 years. There are seven genetic subgroups of XP, which are all resultant of pathogenic mutations in genes in the nucleotide excision repair (NER) pathway and a XP variant resultant of a mutation in translesion synthesis, POLH. The clinical symptoms and severity of the disease is varied across the subgroups, which does not correlate with the functional position of the affected protein in the NER pathway. The aim of this study was to further understand the biology of XP subgroups, particularly those that manifest with neurological symptoms. Whole genome gene expression profiling of fibroblasts from each XP complementation group was assessed before and after UV-light exposure. The biological pathways with altered gene expression after UV-light exposure were distinct for each subtype and contained oncogenic related functions such as perturbation of cell cycle, apoptosis, proliferation and differentiation. Patients from the subgroups XP-B and XP-F were the only subgroups to have transcripts associated with neuronal activity altered after UV-light exposure. This study will assist in furthering our understanding of the different subtypes of XP which will lead to better diagnosis, treatment and management of the disease.

DOI 10.3390/ijms160715985
Citations Scopus - 3Web of Science - 3
Co-authors Nikola Bowden, Rodney Scott
2015 Backer V, Baines KJ, Powell H, Porsbjerg C, Gibson PG, 'Increased asthma and adipose tissue inflammatory gene expression with obesity and Inuit migration to a western country', Respiratory Medicine, (2015) [C1]

© 2015 Elsevier Ltd. Background: An overlap between obesity and asthma exists, and inflammatory cells in adipose tissue could drive the development of asthma. Comparison of adipo... [more]

© 2015 Elsevier Ltd. Background: An overlap between obesity and asthma exists, and inflammatory cells in adipose tissue could drive the development of asthma. Comparison of adipose tissue gene expression among Inuit living in Greenland to those in Denmark provides an opportunity to assess how changes in adipose tissue inflammation can be modified by migration and diet. Objective: To examine mast cell and inflammatory markers in adipose tissue and the association with asthma. Methods: Two Inuit populations were recruited, one living in Greenland and another in Denmark. All underwent adipose subcutaneous biopsy, followed by clinical assessment of asthma, and measurement of AHR. Adipose tissue biopsies were homogenised, RNA extracted, and PCR was performed to determine the relative gene expression of mast cell (tryptase, chymase, CPA3) and inflammatory markers (IL-6, IL-1ß, and CD163). Results: Of the 1059 Greenlandic Inuit participants, 556 were living in Greenland and 6.4% had asthma. Asthma was increased in Denmark (9%) compared to Greenland (3.6%, p < 0.0001) and associated with increased adipose tissue IL-6 gene expression and increased BMI. There was no association between asthma and adipose tissue mast cell gene expression. Pro-inflammatory gene expression (IL-6, IL-1ß) was higher in those living in Denmark, and with increasing BMI and dietary changes. The anti-inflammatory (M2) macrophage marker, CD163, was higher in Greenland-dwelling Inuit (p < 0.01). Conclusions: No association was found between gene expression of mast cell markers in adipose tissue and asthma. Among Greenlandic Inuit, adipose tissue inflammation is also increased in those who migrate to Denmark, possibly as a result of dietary changes.

DOI 10.1016/j.rmed.2015.12.003
Citations Scopus - 1Web of Science - 1
Co-authors Peter Gibson
2015 Gao P, Gibson PG, Baines KJ, Yang IA, Upham JW, Reynolds PN, et al., 'Anti-inflammatory deficiencies in neutrophilic asthma: Reduced galectin-3 and IL-1RA/IL-1ß', Respiratory Research, 16 1-10 (2015) [C1]
DOI 10.1186/s12931-014-0163-5
Citations Scopus - 12Web of Science - 9
Co-authors Jodie Simpson, Peter Gibson
2015 Baines KJ, Wright TK, Simpson JL, McDonald VM, Wood LG, Parsons KS, et al., 'Airway beta-Defensin-1 Protein Is Elevated in COPD and Severe Asthma', MEDIATORS OF INFLAMMATION, (2015) [C1]
DOI 10.1155/2015/407271
Citations Scopus - 4Web of Science - 4
Co-authors Vanessa Mcdonald, Lisa Wood, Peter Wark, Jodie Simpson, Peter Gibson
2014 Simpson JL, Powell H, Baines KJ, Milne D, Coxson HO, Hansbro PM, Gibson PG, 'The Effect of Azithromycin in Adults with Stable Neutrophilic COPD: A Double Blind Randomised, Placebo Controlled Trial', PLOS ONE, 9 (2014) [C1]
DOI 10.1371/journal.pone.0105609
Citations Scopus - 15Web of Science - 12
Co-authors Peter Gibson, Philip Hansbro, Jodie Simpson
2014 Baines KJ, Upham JW, Yerkovich ST, Chang AB, Marchant JM, Carroll M, et al., 'Mediators of neutrophil function in children with protracted bacterial bronchitis', Chest, 146 1013-1020 (2014) [C1]

© 2014 American College of Chest Physicians.BACKGROUND: Protracted bacterial bronchitis (PBB) is a common and treatable cause of chronic wet cough in children in which the mechan... [more]

© 2014 American College of Chest Physicians.BACKGROUND: Protracted bacterial bronchitis (PBB) is a common and treatable cause of chronic wet cough in children in which the mechanisms are not understood. Th is study investigates the IL-1 pathway and a neutrophil gene expression signature in PBB.METHODS: BAL was collected from children in an experimental cohort (n = 21, PBB; n = 33, control subjects), and a second validation cohort (n = 36, PBB; n = 11, control subjects). IL-1ß , IL-1 receptor antagonist (IL-1RA), and a -defensins 1-3 were assayed by enzyme-linked immunosorbent assay, western blot, and quantitative real-time polymerase chain reaction, together with selected IL-1 pathway members and neutrophil-related molecules.RESULTS: In the experimental cohort, children with symptomatic PBB had significantly higher levels of IL-1ß and a -defensin gene and protein expression. Expression of the neutrophil chemokine receptor C-X-C motif receptor 2 was also higher in PBB. IL-1RA protein was higher, however, the IL-1RA:IL-1ß ratio was lower in children with PBB than control subjects. In the validation cohort, protein and gene expression of IL-1ß and a -defensins 1-3 were confirmed higher, as was gene expression of IL-1 pathway members and C-X-C motif receptor 2. IL-1ß and a -defensin 1-3 levels lowered when PBB was treated and resolved. In children with recurrent PBB, gene expression of the IL-1ß signaling molecules pellino-1 and IL-1 receptor-associated kinase 2 was significantly higher. IL-1ß protein levels correlated with BAL neutrophilia and the duration and severity of cough symptoms. IL-1ß and a -defensin 1-3 levels were highly correlated.CONCLUSIONS: PBB is characterized by increased IL-1ß pathway activation. IL-1ß and related mediators were associated with BAL neutrophils, cough symptoms, and disease recurrence, providing insight into PBB pathogenesis.

DOI 10.1378/chest.14-0131
Citations Scopus - 10Web of Science - 11
Co-authors Peter Gibson, Jodie Simpson
2014 Gunawardhana LP, Gibson PG, Simpson JL, Benton MC, Lea RA, Baines KJ, 'Characteristic DNA methylation profiles in peripheral blood monocytes are associated with inflammatory phenotypes of asthma.', Epigenetics, 9 1302-1316 (2014) [C1]
DOI 10.4161/epi.33066
Citations Scopus - 16Web of Science - 13
Co-authors Peter Gibson, Jodie Simpson
2014 Baines KJ, Backer V, Gibson PG, Powel H, Porsbjerg CM, 'Impaired lung function is associated with systemic inflammation and macrophage activation.', The European Respiratory Journal, 45 557-559 (2014) [C1]
Citations Scopus - 6Web of Science - 6
Co-authors Peter Gibson
2014 Simpson JL, Baines KJ, Ryan N, Gibson PG, 'Neutrophilic asthma is characterised by increased rhinosinusitis with sleep disturbance and GERD', Asian Pacific Journal of Allergy and Immunology, 32 66-74 (2014) [C1]

Background: Asthma is a heterogeneous inflammatory disease and eosinophilic, noneosinophilic and neutrophilic forms are recognised. While clinically similar to eosinophilic asthma... [more]

Background: Asthma is a heterogeneous inflammatory disease and eosinophilic, noneosinophilic and neutrophilic forms are recognised. While clinically similar to eosinophilic asthma, patients with non-eosinophilic asthma have different responses to treatment and little is known about the triggers of symptoms and inflammation. Objective: This study sought to characterise asthma control, exacerbation frequency and potential triggers of non-eosinophilic and specifically neutrophilic asthma such as infection, gastroesophageal reflux disease, and rhinosinusitis. Methods: Adults with asthma (n=65; doctor's diagnosis plus demonstrated response to bronchodilator and/or airways hyperresponsiveness to hypertonic saline) were recruited from the Respiratory and Sleep Medicine Ambulatory Care Service at John Hunter Hospital, NSW, Australia. Questionnaires were administered to assess gastroesophageal reflux disease, rhinosinusitis and asthma control. A sputum induction was performed and sputum was processed for assessment of inflammatory cells, infection, and lipid laden macrophages (Oil Red O). Results: Participants with neutrophilic asthma (n=11, 23%) had a higher frequency of primary care doctor visits for asthma exacerbations and a high prevalence (>70%) of chest infections in the previous 12 months. There was also an increased prevalence of rhinosinusitis (64%) and increased symptoms of gastroesophageal reflux disease compared to those with eosinophilic asthma. Conclusions: The clinical pattern of neutrophilic asthma is different from paucigranulocytic and eosinophilic asthma with evidence of abnormal upper airways responses. Specific and targeted treatment of these airway problems may assist in the control and management of neutrophilic asthma.

DOI 10.12932/AP0322.32.1.2014
Citations Scopus - 9Web of Science - 7
Co-authors Peter Gibson, Jodie Simpson, Nicole Ryan
2014 Simpson JL, Phipps S, Baines KJ, Oreo KM, Gunawardhana L, Gibson PG, 'Elevated expression of the NLRP3 inflammasome in neutrophilic asthma', European Respiratory Journal, 43 1067-1076 (2014) [C1]

Asthma is a heterogeneous inflammatory airways disorder where interleukin (IL)-1ß is thought to be a key mediator, especially in the neutrophilic subtype of asthma. The generatio... [more]

Asthma is a heterogeneous inflammatory airways disorder where interleukin (IL)-1ß is thought to be a key mediator, especially in the neutrophilic subtype of asthma. The generation of active IL-1ß requires proteolytic cleavage typically mediated through the formation of a caspase-1-containing inflammasome. This study hypothesised that an IL-1ß endotype associated with the nucleotide-binding domain, leucine-rich repeat-containing family protein (NLRP)3/apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC)/caspase-1 inflammasome is characteristic of patients with the neutrophilic subtype of asthma. Participants with asthma (n=85) and healthy controls (n=27) underwent clinical assessment, spirometry and sputum induction. Sputum was processed for differential cell count, gene expression and protein mediators. NLRP3 and caspase-1 expression was also determined by immunocytochemistry. Sputum macrophages were isolated (n=8) and gene expression of NLRP3 and IL-1ß determined. There was significantly elevated gene expression of NLRP3, caspase-1, caspase-4, caspase-5 and IL-1ß in participants with neutrophilic asthma. Protein levels of IL-1ß were significantly higher in those with neutrophilic asthma and correlated with sputum IL-8 levels. Sputum macrophages, as well as sputum neutrophils in neutrophilic asthma, expressed NLRP3 and caspase-1 protein. NLRP3 inflammasome is upregulated in neutrophilic asthma and may regulate the inflammation process observed in this asthma phenotype through production of IL-1ß. Copyright © ERS 2014.

DOI 10.1183/09031936.00105013
Citations Scopus - 35Web of Science - 34
Co-authors Peter Gibson, Jodie Simpson
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 - 7Web of Science - 6
Co-authors Joerg Mattes, Peter Gibson, Vanessa Murphy
2014 Oreo KM, Gibson PG, Simpson JL, Wood LG, Mcdonald VM, Baines KJ, 'Sputum ADAM8 expression is increased in severe asthma and COPD', Clinical and Experimental Allergy, 44 342-352 (2014) [C1]

Background: Severe asthma and chronic obstructive pulmonary disease (COPD) are chronic inflammatory airway diseases in which the mechanisms are not fully understood. A disintegrin... [more]

Background: Severe asthma and chronic obstructive pulmonary disease (COPD) are chronic inflammatory airway diseases in which the mechanisms are not fully understood. A disintegrin and metalloproteinase domain 8 (ADAM8) is an enzyme expressed on most leucocytes and may be important for facilitating leucocyte migration in respiratory disease. Objective: To investigate ADAM8 mRNA and protein expression in asthma and COPD and its relationship between asthma severity and inflammatory phenotypes. Methods: Induced sputum was collected from 113 subjects with asthma (severe n = 31, uncontrolled n = 39 and controlled n = 35), 20 subjects with COPD and 21 healthy controls. Sputum ADAM8 mRNA expression was measured by qPCR, and soluble ADAM8 (sADAM8) protein was measured in the sputum supernatant by validated ELISA. Results: ADAM8 mRNA correlated with ADAM8 protein levels (r = 0.27, P < 0.01). ADAM8 mRNA (P = 0.004) and sADAM8 protein (P = 0.014) levels were significantly higher in both asthma and COPD compared with healthy controls. ADAM8 mRNA (P = 0.035) and sADAM8 protein (P = 0.002) levels were significantly higher in severe asthma compared with controlled asthma. Total inflammatory cell count (P < 0.01) and neutrophils (P < 0.01) were also elevated in severe asthmatic sputum. Although ADAM8 mRNA was significantly higher in eosinophilic and neutrophilic asthma (P < 0.001), sADAM8 did not differ between asthma inflammatory phenotypes. ADAM8 expression positively correlated with sputum total cell count and sputum neutrophils. Conclusions and Clinical Relevance: ADAM8 expression is increased in both severe asthma and COPD and associated with sputum total cell count and neutrophils. ADAM8 may facilitate neutrophil migration to the airways in severe asthma and COPD. © 2013 John Wiley & Sons Ltd.

DOI 10.1111/cea.12223
Citations Scopus - 6Web of Science - 6
Co-authors Jodie Simpson, Peter Gibson, Vanessa Mcdonald, Lisa Wood
2014 Gunawardhana LP, Gibson PG, Simpson JL, Powell H, Baines KJ, 'Activity and expression of histone acetylases and deacetylases in inflammatory phenotypes of asthma', Clinical & Experimental Allergy, 44 47-57 (2014) [C1]
DOI 10.1111/cea.12168
Citations Scopus - 15Web of Science - 15
Co-authors Jodie Simpson, Peter Gibson
2014 Baines KJ, Simpson JL, Wood LG, Scott RJ, Fibbens NL, Powell H, et al., 'Sputum gene expression signature of 6 biomarkers discriminates asthma inflammatory phenotypes', Journal of Allergy and Clinical Immunology, 133 997-1007 (2014) [C1]

Background Airway inflammation is associated with asthma exacerbation risk, treatment response, and disease mechanisms. Objective This study aimed to identify and validate a sputu... [more]

Background Airway inflammation is associated with asthma exacerbation risk, treatment response, and disease mechanisms. Objective This study aimed to identify and validate a sputum gene expression signature that discriminates asthma inflammatory phenotypes. Methods An asthma phenotype biomarker discovery study generated gene expression profiles from induced sputum of 47 asthmatic patients. A clinical validation study (n = 59 asthmatic patients) confirmed differential expression of key genes. A 6-gene signature was identified and evaluated for reproducibility (n = 30 asthmatic patients and n = 20 control subjects) and prediction of inhaled corticosteroid (ICS) response (n = 71 asthmatic patients). Receiver operating characteristic curves were calculated, and area under the curve (AUC) values were reported. Results From 277 differentially expressed genes between asthma inflammatory phenotypes, we identified 23 genes that showed highly significant differential expression in both the discovery and validation populations. A signature of 6 genes, including Charcot-Leydon crystal protein (CLC); carboxypeptidase A3 (CPA3); deoxyribonuclease I-like 3 (DNASE1L3); IL-1ß (IL1B); alkaline phosphatase, tissue-nonspecific isozyme (ALPL); and chemokine (C-X-C motif) receptor 2 (CXCR2), was reproducible and could significantly (P <.0001) discriminate eosinophilic asthma from other phenotypes, including patients with noneosinophilic asthma (AUC, 89.6%), paucigranulocytic asthma (AUC, 92.6%), or neutrophilic asthma (AUC, 91.4%) and healthy control subjects (AUC, 97.6%), as well as discriminating patients with neutrophilic asthma from those with paucigranulocytic asthma (AUC, 85.7%) and healthy control subjects (AUC, 90.8). The 6-gene signature predicted ICS response (>12% change in FEV1; AUC, 91.5%). ICS treatment reduced the expression of CLC, CPA3, and DNASE1L3 in patients with eosinophilic asthma. Conclusions A sputum gene expression signature of 6 biomarkers reproducibly and significantly discriminates inflammatory phenotypes of asthma and predicts ICS treatment response. This signature has the potential to become a useful diagnostic tool to assist in the clinical diagnosis and management of asthma. © 2013 American Academy of Allergy, Asthma & Immunology.

DOI 10.1016/j.jaci.2013.12.1091
Citations Scopus - 49Web of Science - 49
Co-authors Lisa Wood, Peter Gibson, Jodie Simpson, Rodney Scott
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 - 8Web of Science - 8
Co-authors Joerg Mattes, Peter Gibson, Vanessa Murphy, Jodie Simpson
2014 Baines KJ, Pavord ID, Gibson PG, 'The role of biomarkers in the management of airways disease.', Int J Tuberc Lung Dis, 18 1264-1268 (2014) [C1]
DOI 10.5588/ijtld.14.0226
Citations Scopus - 11Web of Science - 7
Co-authors Peter Gibson
2013 Kaiko GE, Loh Z, Spann K, Lynch JP, Lalwani A, Zheng Z, et al., 'Toll-like receptor 7 gene deficiency and early-life Pneumovirus infection interact to predispose toward the development of asthma-like pathology in mice', JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 131 1331-U132 (2013) [C1]
DOI 10.1016/j.jaci.2013.02.041
Citations Scopus - 27Web of Science - 26
Co-authors Paul Foster, Jodie Simpson
2013 Simpson JL, McDonald VM, Baines KJ, Oreo KM, Wang F, Hansbro PM, Gibson PG, 'Influence of Age, Past Smoking, and Disease Severity on TLR2, Neutrophilic Inflammation, and MMP-9 Levels in COPD', MEDIATORS OF INFLAMMATION, (2013) [C1]
DOI 10.1155/2013/462934
Citations Scopus - 14Web of Science - 14
Co-authors Philip Hansbro, Peter Gibson, Jodie Simpson, Vanessa Mcdonald
2013 Baines KJ, Hsu AC-Y, Tooze M, Gunawardhana LP, Gibson PG, Wark PAB, 'Novel immune genes associated with excessive inflammatory and antiviral responses to rhinovirus in COPD', RESPIRATORY RESEARCH, 14 (2013) [C1]
DOI 10.1186/1465-9921-14-15
Citations Scopus - 15Web of Science - 16
Co-authors Alan Hsu, Peter Wark, Peter Gibson
2013 Fu J-J, Baines KJ, Wood LG, Gibson PG, 'Systemic Inflammation Is Associated with Differential Gene Expression and Airway Neutrophilia in Asthma', OMICS-A JOURNAL OF INTEGRATIVE BIOLOGY, 17 187-199 (2013) [C1]
DOI 10.1089/omi.2012.0104
Citations Scopus - 23Web of Science - 19
Co-authors Lisa Wood, Peter Gibson
2012 Wood LG, Baines KJ, Fu J, Scott HA, Gibson PG, 'The neutrophilic inflammatory phenotype is associated with systemic inflammation in asthma', Chest, 142 86-93 (2012) [C1]
Citations Scopus - 100Web of Science - 92
Co-authors Peter Gibson, Lisa Wood, Hayley Scott
2011 Baines KJ, Simpson JL, Gibson PG, 'Innate immune responses are increased in chronic obstructive pulmonary disease', PLoS ONE, 36 e18426 (2011) [C1]
DOI 10.1371/journal.pone.0018426
Citations Scopus - 40Web of Science - 31
Co-authors Peter Gibson, Jodie Simpson
2011 Baines KJ, Simpson JL, Wood LG, Scott R, Gibson PG, 'Systemic upregulation of neutrophil a-defensins and serine proteases in neutrophilic asthma', Thorax, 66 942-947 (2011) [C1]
Citations Scopus - 34Web of Science - 31
Co-authors Peter Gibson, Lisa Wood, Rodney Scott, Jodie Simpson
2011 Baines KJ, Simpson JL, Wood LG, Scott R, Gibson PG, 'Transcriptional phenotypes of asthma defined by gene expression profiling of induced sputum samples', Journal of Allergy and Clinical Immunology, 127 153.e9-160.e9 (2011) [C1]
DOI 10.1016/j.jaci.2010.10.024
Citations Scopus - 102Web of Science - 89
Co-authors Rodney Scott, Jodie Simpson, Peter Gibson, Lisa Wood
2011 Wang F, He XY, Baines KJ, Gunawardhana LP, Simpson JL, Li F, Gibson PG, 'Different inflammatory phenotypes in adults and children with acute asthma', European Respiratory Journal, 38 567-574 (2011) [C1]
DOI 10.1183/09031936.00170110
Citations Scopus - 38Web of Science - 34
Co-authors Jodie Simpson, Peter Gibson
2010 Li J, Wang W, Baines KJ, Bowden NA, Hansbro PM, Gibson PG, et al., 'IL-27/IFN-y induce MyD88-dependent steroid-resistant airway hyperresponsiveness by inhibiting glucocorticoid signaling in macrophages', Journal of Immunology, 185 4401-4409 (2010) [C1]
DOI 10.4049/jimmunol.1001039
Citations Scopus - 52Web of Science - 47
Co-authors Nikola Bowden, Ming Yang, Peter Gibson, Paul Foster, Philip Hansbro
2010 Baines KJ, Simpson JL, Bowden NA, Scott R, Gibson PG, 'Differential gene expression and cytokine production from neutrophils in asthma phenotypes', European Respiratory Journal, 35 522-531 (2010) [C1]
DOI 10.1183/09031936.00027409
Citations Scopus - 42Web of Science - 34
Co-authors Rodney Scott, Peter Gibson, Jodie Simpson, Nikola Bowden
2009 Baines KJ, Wood LG, Gibson PG, 'The nutrigenomics of asthma: Molecular mechanisms of airway neutrophilia following dietary antioxidant withdrawal', OMICS: A Journal of Integrative Biology, 13 355-365 (2009) [C1]
DOI 10.1089/omi.2009.0042
Citations Scopus - 17Web of Science - 12
Co-authors Lisa Wood, Peter Gibson
2009 Baines KJ, Simpson JL, Scott R, Gibson PG, 'Immune responses of airway neutrophils are impaired in asthma', Experimental Lung Research, 35 554-569 (2009) [C1]
DOI 10.1080/01902140902777490
Citations Scopus - 20Web of Science - 19
Co-authors Peter Gibson, Jodie Simpson, Rodney Scott
2009 Simpson JL, Baines KJ, Boyle MJ, Scott R, Gibson PG, 'Oncostatin M (OSM) is increased in asthma with incompletely reversible airflow obstruction', Experimental Lung Research, 35 781-794 (2009) [C1]
DOI 10.3109/01902140902906412
Citations Scopus - 19Web of Science - 19
Co-authors Peter Gibson, Jodie Simpson, Rodney Scott
Show 51 more journal articles

Conference (75 outputs)

Year Citation Altmetrics Link
2017 Wood LG, Berthon BS, Zapirain R, Leong LEX, Baines KJ, Gibson PG, et al., 'ASTHMA CONTROL, AIRWAY INFLAMMATION AND GUT MICROBIOME ARE IMPROVED BY SOLUBLE FIBRE SUPPLEMENTATION', RESPIROLOGY (2017)
Co-authors Lisa Wood
2017 Pabreja K, Gibson PG, Baines KJ, Eyers F, Yang M, Nair P, et al., 'INCREASED EXPRESSION OF IL-27 IN NEUTROPHILIC ASTHMA', RESPIROLOGY (2017)
Co-authors Peter Gibson, Jodie Simpson
2017 Sanchez S, Wark P, Baines K, Simpson J, 'ASTHMA GENE SIGNATURES EXPRESSION IN BRONCHIAL BIOPSY', RESPIROLOGY (2017)
Co-authors Jodie Simpson, Peter Wark
2017 Nguyen TH, Maltby S, Simpson JL, Eyers F, Baines KJ, Gibson PG, et al., 'MACROPHAGES REGULATE THE DEVELOPMENT OF RSV INDUCED ASTHMA EXACERBATIONS', RESPIROLOGY (2017)
Co-authors Jodie Simpson, Peter Gibson, Steven Maltby
2017 Wood LG, Li Q, Berthon BS, Gibson PG, Baines KJ, 'SATURATED FATTY ACIDS, BUT NOT N-6 POLYUNSATURATED FATTY ACIDS OR CARBOHYDRATES, INCREASE AIRWAY INFLAMMATION IN NON-OBESE ASTHMATICS', RESPIROLOGY (2017)
Co-authors Lisa Wood, Peter Gibson
2017 McDonald VM, Clark VL, Wark PAB, Baines KJ, Gibson PG, 'MULTIDIMENSIONAL ASSESSMENT AND TARGETED THERAPY OF SEVERE PERSISTENT ASTHMA: A RANDOMISED CONTROLLED TRIAL', RESPIROLOGY (2017)
Co-authors Vanessa Mcdonald, Peter Wark, Peter Gibson
2016 Negewo N, Gibson, Wood, Baines, McDonald, 'Effect of weight loss on COPD-associated comorbidities in obese COPD' (2016)
DOI 10.1183/13993003.congress-2016.PA643
Co-authors Lisa Wood, Vanessa Mcdonald
2016 Kim RY, Pinkerton JW, Essilfie A-T, Robertson AA, Baines KJ, Mayall JR, et al., 'Nlrp3 Inflammasome-Mediated, Il-1 beta-Dependent Inflammatory Responses Drive Severe, Steroid-Insensitive Asthma', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2016)
Co-authors Peter Wark, Philip Hansbro, Peter Gibson, Jay Horvat, Malcolm Starkey
2015 Tang F, Hansbro P, Burgess J, Baines K, Oliver B, 'NEUTROPHILS DISPLAY IMMUNOREGULATORY ROLES IN RHINOVIRUS INFECTIONS', RESPIROLOGY (2015) [E3]
Co-authors Philip Hansbro
2015 Upham J, Chen A, Carroll M, Petsky H, Pizzutto S, Yerkovich S, et al., 'IMMUNE RESPONSES TO NONTYPEABLE HAEMOPHILUS INFLUENZAE IN PROTRACTED BACTERIAL BRONCHITIS', RESPIROLOGY (2015) [E3]
Citations Web of Science - 1
Co-authors Jodie Simpson, Peter Gibson
2015 Baines K, Wright T, Simpson J, Mcdonald V, Wood L, Gibson P, 'EXCESSIVE NEUTROPHIL EXTRACELLULAR TRAPS ARE ASSOCIATED WITH INFLAMMATION IN CHRONIC AIRWAY DISEASE', RESPIROLOGY (2015) [E3]
Co-authors Peter Gibson, Lisa Wood, Jodie Simpson, Vanessa Mcdonald
2015 Erriah M, Gao P, Baines K, Gibson P, Simpson J, 'SPUTUM GALECTIN-3 EXPRESSION IS ASSOCIATED WITH EOSINOPHILS IN COPD', RESPIROLOGY (2015) [E3]
Co-authors Jodie Simpson, Peter Gibson
2015 Upham JW, Chang A, Pizzutto S, Carroll M, Gibson P, Simpson J, et al., 'Immune Responses To Non-Typeable Haemophilus Influenzae In Protracted Bacterial Bronchitis', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2015)
Co-authors Jodie Simpson, Peter Gibson
2015 McDonald V, Wark P, Baines K, Gibson P, 'A multidimensional assessment of severe asthma', American Journal of Respiratory and Critical Care Medicine (2015) [E3]
Co-authors Peter Wark, Vanessa Mcdonald, Peter Gibson
2015 Tang F, Gibson P, Foxley G, Burgess J, Baines K, Oliver B, 'Neutrophils from people with uncontrolled asthma have a deficient CXCL8 response to bacteria but not to viruses', Am J Resp Crit Care Med (2015) [E3]
Co-authors Peter Gibson
2015 Baines K, Wright T, Simpson J, McDonald V, Wood L, Gibson P, 'Accumulation of neutrophil extracellular traps is associated with inflammation in neutrophilic asthma and COPD', Am J Resp Crit Care Med (2015) [E3]
Co-authors Jodie Simpson, Vanessa Mcdonald, Lisa Wood, Peter Gibson
2015 McDonald V, Wark P, Baines K, Gibson P, 'The multidimensional components of severe asthma', Respirology (2015) [E3]
Co-authors Vanessa Mcdonald, Peter Gibson, Peter Wark
2015 Tang F, Gibson P, Foxley G, Burgess J, Baines K, Oliver B, 'Deficient CXCL8 response to bacteria but not to viruses in neutrophils from people with uncontrolled asthma', Respirology (2015) [E3]
Co-authors Peter Gibson
2015 Tang F, Hansbro P, Burgess J, Baines K, Oliver B, 'A novel immunoregulatory role of neutrophils in viral infections', American Journal of Respiratory and Critical Care Medicine (2015) [E3]
Co-authors Philip Hansbro
2015 Negewo N, McDonald V, Baines K, Wark P, Simpson J, Jones P, Gibson P, 'Can blood eosinophils predict sputum eosinophils in stable COPD?' (2015)
DOI 10.1183/13993003.congress-2015.PA3967
Co-authors Jodie Simpson, Peter Wark, Vanessa Mcdonald, Peter Gibson
2014 Tang F, Van Ly D, Reading P, Spann K, Hartl D, Burgess JK, et al., 'Neutrophils Respond To Viral Surrogates And Respiratory Viruses', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2014)
2014 Fu J-J, McDonald VM, Baines KJ, Mao B, Gibson PG, 'Airway Il-1 Pathway Activation And Systemic Inflammation Predict Future Exacerbation Risk In Asthma And COPD', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2014)
Co-authors Vanessa Mcdonald, Peter Gibson
2014 Baines KJ, Simpson JL, Wood LG, Scott RJ, Fibbens NL, Powell H, et al., 'An Expression Signature Of 6 Genes Can Reliably Distinguish Eosinophilic And Neutrophilic Inflammation And Corticosteroid Response In Asthma', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2014)
Co-authors Jodie Simpson, Rodney Scott, Peter Gibson, Lisa Wood
2014 Wright T, Gibson P, Simpson J, Mcdonald V, Wood L, Baines K, 'ALARMINS IN ASTHMA AND COPD: RELATIONSHIPS TO INFLAMMATORY PHENOTYPES AND DISEASE SEVERITY', RESPIROLOGY (2014) [E3]
Co-authors Lisa Wood, Jodie Simpson, Peter Gibson, Vanessa Mcdonald
2014 Baines K, Simpson J, Wood L, Scott R, Fibbens N, Powell H, et al., 'SPUTUM GENE EXPRESSION OF SIX MARKERS IDENTIFIES ASTHMA INFLAMMATORY PHENOTYPE AND CORTICOSTEROID RESPONSE', RESPIROLOGY (2014) [E3]
Co-authors Rodney Scott, Peter Gibson, Jodie Simpson, Lisa Wood
2014 Baines K, Upham J, Yerkovich S, Chang A, Marchant J, Carroll M, et al., 'INTERLEUKIN-1B IS RELATED TO CLINICAL OUTCOMES IN PROTRACTED BACTERIAL BRONCHITIS', RESPIROLOGY (2014) [E3]
Co-authors Peter Gibson, Jodie Simpson
2014 Simpson J, Gao P, Baines K, Yang I, Reynolds P, Hodge S, et al., 'GALECTIN 3 AND GALECTIN 3 BINDING PROTEIN IN ASTHMA INFLAMMATORY SUBTYPES', RESPIROLOGY (2014) [E3]
Co-authors Jodie Simpson, Peter Gibson
2014 Baines K, Backer V, Gibson P, Powell H, Porsbjerg C, 'Systemic inflammation, diet, and place of residence modify lung function in Greenland Inuit.', Eur Resp J (2014)
2014 Sverrild A, Baines K, Backer V, Gibson P, Porsbjerg C, 'Increased IL-33 expression is related to high levels of TLR-2 and -4 in steroid-free subjects with asthma', Eur Resp J (2014)
2014 Porsbjerg C, Baines K, Sverrild A, Backer V, Gibson P, 'Eosinophilic airway inflammation is associated with increased TLR2 and TLR4 expression in adult asthmatics.', Eur Resp J (2014)
2014 Tang F, Van Ly D, Reading P, Baines KJ, Spann K, Burgess J, et al., 'Viral surrogates and respiratory viruses differentially activate neutrophils', Respirology (2014)
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 Vanessa Murphy, Peter Gibson, Joerg Mattes, Jodie Simpson
2013 Simpson JL, Baines KJ, Ryan NM, Gibson PG, 'NEUTROPHILIC ASTHMA IS CHARACTERIZED BY INCREASED GERD AND RHINOSINUSITIS WITH SLEEP DISTURBANCE', RESPIROLOGY (2013) [E3]
Co-authors Peter Gibson, Nicole Ryan, Jodie Simpson
2013 Baines KJ, Simpson JL, Mcdonald VM, Hsu AC, Gibson PG, 'DIFFERENTIAL AIRWAY GENE EXPRESSION IN COPD', RESPIROLOGY (2013) [E3]
Co-authors Peter Gibson, Jodie Simpson, Vanessa Mcdonald, Alan Hsu
2013 Wang G, Baines KJ, Fu JJ, Gibson PG, 'MAST CELL-BASED PHENOTYPES OF ASTHMA IN INDUCED SPUTUM SAMPLES', RESPIROLOGY (2013) [E3]
Citations Web of Science - 1
Co-authors Peter Gibson
2013 Baines KJ, Simpson JL, Wood LG, Scott RJ, Fibbens NL, Powell H, et al., 'Sputum gene expression of six markers identifies asthma inflammatory phenotype and corticosteroid response.', Australasian Genomic Technologies Association Annual Scientific Meeting, Gold Coast, QLD (2013)
2013 Baines KJ, Upham JW, Yerkovich ST, Chang AB, Marchant J, Carroll M, et al., 'Interleukin-1ß is related to clinical outcomes in protracted bacterial bronchitis', Australasian Society for Immunology, Wellington, NZ (2013)
2012 Simpson JL, Phipps S, Baines KJ, Oreo KM, Gibson PG, 'NALP3 INFLAMMASOME ACTIVATION IN NEUTROPHILIC ASTHMA', RESPIROLOGY (2012) [E3]
Co-authors Jodie Simpson, Peter Gibson
2012 Simpson JL, Phipps S, Baines KJ, Oreo K, Gibson PG, 'NALP3 inflammasome activation in neutrophilic asthma', Respirology (2012) [E3]
Co-authors Jodie Simpson, Peter Gibson
2012 Baines KJ, Simpson JL, Wood LG, Scott RJ, Gibson PG, 'Sputum gene expression of mast cell specific proteases are increased in eosinophilic asthma', Respirology (2012) [E3]
Co-authors Peter Gibson, Lisa Wood, Rodney Scott, Jodie Simpson
2012 Baines KJ, Simpson JL, Wood LG, Scott RJ, Gibson PG, 'Induced sputum differential gene expression implicates increased p38 signalling activity in severe asthma', Respirology (2012) [E3]
Co-authors Rodney Scott, Lisa Wood, Jodie Simpson, Peter Gibson
2011 Baines KJ, Simpson JL, Scott R, Wood LG, Gibson PG, 'Systemic upregulation of neutrophil a-defensins and serine proteases in neutrophilic asthma', European Respiratory Society Annual Congress 2011 Abstracts (2011) [E3]
Co-authors Lisa Wood, Jodie Simpson, Rodney Scott, Peter Gibson
2011 Baines KJ, Simpson JL, Scott R, Wood LG, Gibson PG, 'Sputum gene expression of mast cell tryptase and carboxypeptidase A3 are increased in eosinophilic asthma', European Respiratory Society Annual Congress 2011 Abstracts (2011) [E3]
Co-authors Rodney Scott, Peter Gibson, Lisa Wood, Jodie Simpson
2011 Baines KJ, Simpson JL, Scott R, Wood LG, Gibson PG, 'Induced sputum differential gene expression implicates increased p38 signalling activity in severe asthma', European Respiratory Society Annual Congress 2011 Abstracts (2011) [E3]
Co-authors Peter Gibson, Jodie Simpson, Lisa Wood, Rodney Scott
2011 Baines KJ, Simpson JL, Scott RJ, Wood LG, Gibson PG, 'Analysis of systemic gene expression according to inflammatory phenotype of asthma.', Respirology (2011)
2011 Oliver BG, Tang FS, Van Ly D, Burgess JK, Black JL, Baines KJ, 'Imiquimod, poly I:c and rhinovirus induce interleukin (iL)-6 and IL-8 release from polymorphonuclear cells and peripheral blood mononuclear cells: Effect of dexamethasone', American Journal of Respiratory and Critical Care Medicine (2011) [E3]
2011 Baines KJ, Simpson JL, Scott R, Wood LG, Gibson PG, 'Analysis of systemic gene expression according to inflammatory phenotype of asthma', Respirology (2011) [E3]
Co-authors Lisa Wood, Peter Gibson, Jodie Simpson, Rodney Scott
2011 Baines KJ, Tooze MK, Wark PA, 'Rhinovirus infected airway epithelial cells have an increased pro-inflammatory response in COPD', Respirology (2011) [E3]
Co-authors Peter Wark
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 (2011) [E3]
Co-authors Joerg Mattes, Jodie Simpson, Peter Gibson, Vanessa Murphy
2011 Oreo K, Baines KJ, Gibson PG, Hansbro PM, 'Pro-inflammatory cytokine production is impaired in response to TLR2 activation in healthy ageing and COPD', Respirology (2011) [E3]
Co-authors Philip Hansbro, Peter Gibson
2011 Wang F, Xy HA, Baines KJ, Gunawardhana LP, Simpson JL, Ki F, Gibson PG, 'Is chalamydophyla a pneumoniae infection related to non-eosinophilic asthma?', Respirology (2011) [E3]
Co-authors Peter Gibson, Jodie Simpson
2011 Fu J, Baines KJ, Wood LG, Scott HA, Gibson PG, 'Low-grade systemic inflammation is associated with airway neutrophilia in asthma', Respirology (2011) [E3]
Co-authors Hayley Scott, Peter Gibson, Lisa Wood
2011 Fu J, Baines KJ, Gibson PG, Scott HA, Wood LG, 'Systemic inflammation mediates airway neutrophilia via the regulation of IL-8 receptor mRNA expression', Respirology (2011) [E3]
Co-authors Peter Gibson, Hayley Scott, Lisa Wood
2010 Baines KJ, Simpson JL, Scott R, Wood LG, Gibson PG, 'Molecular phenotypes of asthma defined by gene expression profiling', American Journal of Respiratory and Critical Care Medicine (2010) [E3]
Co-authors Lisa Wood, Jodie Simpson, Rodney Scott, Peter Gibson
2010 Baines KJ, Simpson JL, Scott R, Wood LG, Gibson PG, 'Analysis of systemic gene expression according to inflammatory phenotype of asthma', Biomarker Discovery Conference (2010) [E3]
Co-authors Lisa Wood, Jodie Simpson, Rodney Scott, Peter Gibson
2010 Gunawardhana LG, Baines KJ, Simpson JL, Mattes J, Murphy VE, Gibson PG, (Oral) BDCD2010, 'Maternal asthma is associated with alterations in DNA methylation profile of peripheral blood of infants.', Biomarker Discovery Conference, Shoal Bay, NSW (2010)
2010 Baines KJ, Simpson JL, Scott R, Wood LG, Gibson PG, 'Molecular phenotypes of asthma defined by gene expression profiling', Respirology (2010) [E3]
Co-authors Jodie Simpson, Rodney Scott, Lisa Wood, Peter Gibson
2009 Baines KJ, Simpson JL, Scott R, Wood LG, Gibson PG, 'Genome wide gene expression of induced sputum in non-eosinophilic asthma', AMATA 2009 (2009) [E3]
Co-authors Lisa Wood, Jodie Simpson, Rodney Scott, Peter Gibson
2009 Bowden NA, Ashton KA, Stibbard GJ, Cox MB, Baines KJ, Scott R, 'Predicting xeroderma pigmentosum complementation group by gene expression profiling', AMATA 2009 (2009) [E3]
Co-authors Nikola Bowden, Rodney Scott
2009 Baines KJ, Grissell TV, Gibson PG, Wark PA, 'Molecular mechanisms of rhinovirus infection of primary bronchial epithelial cells', Respirology (2009) [E3]
DOI 10.1111/j.1440-1843.2009.01503_1.x
Co-authors Peter Gibson, Peter Wark
2009 Baines KJ, Wood LG, Gibson PG, 'Molecular mechanisms of airway neutrophilia following a low antioxidant diet', Respirology (2009) [E3]
DOI 10.1111/j.1440-1843.2009.01503_1.x
Co-authors Lisa Wood, Peter Gibson
2009 Oreo K, Baines KJ, Gibson PG, Hansbro PM, Simpson JL, 'Toll-like receptor agonists stimulate cytokine release from blood but not airway cells', Respirology (2009) [E3]
DOI 10.1111/j.1440-1843.2009.01503_1.x
Co-authors Jodie Simpson, Peter Gibson, Philip Hansbro
2008 Baines KJ, Simpson JL, Scott R, Gibson PG, 'Ageing alters airway and circulating neutrophil function', Respirology (2008) [E3]
DOI 10.1111/j.1440-1843.2008.01252.x
Co-authors Jodie Simpson, Rodney Scott, Peter Gibson
2008 Baines KJ, Simpson JL, Scott R, Gibson PG, 'Innate immune responses of airway neutrophils are impaired in neutrophilic asthma', Respirology (2008) [E3]
DOI 10.1111/j.1440-1843.2008.01252.x
Co-authors Peter Gibson, Rodney Scott, Jodie Simpson
2008 Bowden NA, Baines KJ, Cox MB, Scott R, 'Altered gene expression in nucleotide excision repair deficient fibroblasts after UV-light exposure', AACR Meeting Abstracts (2008) [E3]
Co-authors Rodney Scott, Nikola Bowden
2008 Bowden NA, Baines KJ, Cox MB, Scott R, 'Response to uv-light exposure in fibroblasts with differential nucleotide excision repair capacity', ASMR XVII NSW Scientific Meeting: Programme and Abstracts (2008) [E3]
Co-authors Nikola Bowden, Rodney Scott
2008 Bowden NA, Ashton KA, Baines KJ, Cox MB, Scott R, 'Altered gene expression after UV-light induced DNA damage', Conference on Translational Cancer Research: Abstracts (2008) [E3]
Co-authors Rodney Scott, Nikola Bowden
2008 Baines KJ, Simpson JL, Scott RJ, Gibson PG, 'Innate Immune Responses of Neutrophils are Impaired in Neutrophilic Asthma', Am J Resp Crit Care Med (2008)
2008 Baines KJ, Simpson JL, Scott RJ, Gibson PG, 'Ageing Alters Airway and Circulating Neutrophil Function.', Am J Resp Crit Care Med (2008)
2008 Baines KJ, Simpson JL, Scott RJ, Gibson PG, 'Ageing Alters Airway and Circulating Neutrophil Function', Respirology (2008)
2007 Baines KJ, Bowden NA, Scott R, Simpson JL, Gibson PG, 'Molecular analysis of neutrophils in asthma subtypes', Respirology (TSANZ Abstracts-Posters) (2007) [E3]
DOI 10.1111/j.1440-1843.2007.001050.x
Co-authors Nikola Bowden, Peter Gibson, Rodney Scott, Jodie Simpson
2007 Baines KJ, Bowden NA, Scott RJ, Simpson JL, Gibson PG, 'Molecular Analysis of Neutrophils in Asthma Subtypes', Am J Resp Crit Care Med (2007)
2007 Gibson PG, Baines KJ, Simpson JL, Scott RJ, 'Gene Expression Profiling Identifies Neutrophilic and Eosinophilic Asthma as Distinct Subtypes.', Eur Resp J (2007)
2006 Baines KJ, Simpson JL, Scott R, Bell NV, Boyle MJ, Gibson PG, 'Enhanced IL-8 release from neutrophils in non-eosinophilic asthma', Respirology (2006) [E3]
Co-authors Peter Gibson, Jodie Simpson, Rodney Scott
2005 Baines KJ, Bell NV, Simpson JL, Scott RJ, Boyle MJ, Gibson PG, 'Enhanced IL-8 Release from Neutrophils in Non-Eosinophilic Asthma', Inflammation Research (2005)
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Grants and Funding

Summary

Number of grants 39
Total funding $3,249,359

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


20172 grants / $610,463

Targeting neutrophil extracellular traps to reduce inflammation in severe asthma$590,463

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Doctor Katie Baines, Conjoint Professor Peter Gibson, Professor Jodie Simpson, Professor Dominik Hartl, Professor Vanessa McDonald
Scheme Project Grant
Role Lead
Funding Start 2017
Funding Finish 2019
GNo G1500231
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

Extracellular DNA in pleural fluid as a determinant of empyema pathology and treatment response$20,000

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Doctor Scott Twaddell, Doctor Katie Baines
Scheme Research Grant
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1700745
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

20163 grants / $600,943

Galectin-3 and phagocyte function in severe asthma$420,943

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Jodie Simpson, Doctor Katie Baines, Doctor Jay Horvat, Dr Johan Bylund
Scheme Project Grant
Role Investigator
Funding Start 2016
Funding Finish 2018
GNo G1500194
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

Targeting neutrophil extracellular traps as a novel therapeutic option in COPD$160,000

Funding body: Lung Foundation Australia

Funding body Lung Foundation Australia
Project Team Doctor Katie Baines
Scheme Boehringer Ingelheim Chronic Obstructive Pulmonary Disease Research Fellowship
Role Lead
Funding Start 2016
Funding Finish 2020
GNo G1500407
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

A sputum gene expression signature of 6 biomarkers can predict azithromycin treatment responsiveness and future frequent exacerbations in severe asthma$20,000

Funding body: National Clinical CRE in Severe Asthma

Funding body National Clinical CRE in Severe Asthma
Project Team Doctor Katie Baines
Scheme Seed Research Project
Role Lead
Funding Start 2016
Funding Finish 2016
GNo G1600443
Type Of Funding Internal
Category INTE
UON Y

20153 grants / $155,222

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

Targeting neutrophil extracellular traps as a novel therapeutic option in COPD$25,222

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Doctor Katie Baines, Conjoint Professor Peter Gibson
Scheme Research Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1500570
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

(PROJECT)$10,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Vanessa McDonald, Mrs Netsanet Negewo, Conjoint Professor Peter Gibson, Doctor Katie Baines
Scheme Jennie Thomas Medical Research Travel Grant
Role Investigator
Funding Start 2015
Funding Finish 2015
GNo G1501430
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20146 grants / $269,397

Greenland Study$140,000

Funding body: Bispebjerg Hospital

Funding body Bispebjerg Hospital
Project Team Conjoint Professor Peter Gibson, Doctor Katie Baines, Professor Vibeke Backer
Scheme International Collaboration
Role Investigator
Funding Start 2014
Funding Finish 2016
GNo G1400539
Type Of Funding International - Non Competitive
Category 3IFB
UON Y

Identifying biomarkers that predict severe asthma exacerbations during pregnancy$60,000

Funding body: Thoracic Society of Australia and New Zealand

Funding body Thoracic Society of Australia and New Zealand
Project Team Doctor Katie Baines
Scheme TSANZ/National Asthma Council Australia - Asthma and Airways Career Development Fellowship
Role Lead
Funding Start 2014
Funding Finish 2014
GNo G1400730
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Identifying biomarkers that predict severe asthma exacerbations during pregnancy$27,512

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Doctor Katie Baines, Emeritus Professor Michael Hensley
Scheme Research Grant
Role Lead
Funding Start 2014
Funding Finish 2014
GNo G1400631
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

The role of comorbidities and inflammation in Chronic Obstructive Pulmonary Disease (COPD)$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Mrs Netsanet Negewo, Professor Vanessa McDonald, Conjoint Professor Peter Gibson, Doctor Katie Baines
Scheme Postgraduate Research Scholarship
Role Investigator
Funding Start 2014
Funding Finish 2015
GNo G1401393
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Predicting who is at risk of worsening lung disease in Cystic Fibrosis$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Conjoint Professor Peter Wark, Doctor Katie Baines, Professor Vanessa McDonald, Conjoint Professor Peter Gibson, Associate Professor Scott Bell, Dr David Reid
Scheme Project Grant
Role Investigator
Funding Start 2014
Funding Finish 2014
GNo G1401410
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Thoracic Society of Australia and New Zealand, Adelaide Australia, 4-9 April 2014$1,885

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

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Katie Baines
Scheme Travel Grant
Role Lead
Funding Start 2014
Funding Finish 2014
GNo G1400186
Type Of Funding Internal
Category INTE
UON Y

20135 grants / $598,830

Gene Expression Biomarkers Predict Severe Asthma Inflammatory Phenotype, Activation Mechanisms and Treatment Response$465,629

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Doctor Katie Baines, Conjoint Professor Peter Gibson, Professor Jodie Simpson
Scheme Project Grant
Role Lead
Funding Start 2013
Funding Finish 2015
GNo G1200188
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

Protracted bacterial bronchitis: long term outcomes, systemic and airway predictors of recurrence$86,526

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Anne Chang, Professor John Upham, Conjoint Professor Peter Gibson, Dr Stephanie Yerkovich, Doctor Katie Baines, Dr Sandra Hodge, Mrs Susan Pizzuto, Associate Professor Ian Masters, Dr Helen Buntain
Scheme Project Grant
Role Investigator
Funding Start 2013
Funding Finish 2016
GNo G1200534
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

BD FACSCanto II Violet Laser (405nm) upgrade including Trigon and 2 photomultiplier tubes (PMTs)$25,000

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Conjoint Professor Peter Wark, Doctor Alan Hsu, Doctor Katie Baines, Professor Jodie Simpson, Conjoint Professor Peter Gibson, Ms Hayley See
Scheme Equipment Grant
Role Investigator
Funding Start 2013
Funding Finish 2013
GNo G1201180
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
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, Doctor Jay Horvat, Associate 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

Thoracic Society of Australia and New Zealand$1,675

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

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Katie Baines
Scheme Travel Grant
Role Lead
Funding Start 2013
Funding Finish 2013
GNo G1300405
Type Of Funding Internal
Category INTE
UON Y

20125 grants / $435,832

2011 Research Fellowship - PRCARD$333,302

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Doctor Katie Baines
Scheme Research Fellowship
Role Lead
Funding Start 2012
Funding Finish 2014
GNo G1200356
Type Of Funding Internal
Category INTE
UON Y

Phenotype based management of severe persistent asthma$34,454

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Professor Vanessa McDonald, Doctor Katie Baines, Conjoint Professor Peter Gibson
Scheme Research Grant
Role Investigator
Funding Start 2012
Funding Finish 2012
GNo G1200211
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

Body plethysmograph respiratory function system$33,076

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Conjoint Professor Peter Gibson, Conjoint Professor Peter Wark, Professor Lisa Wood, Professor Jodie Simpson, Doctor Katie Baines, Doctor Vanessa Murphy, Doctor Jeffrey Pretto, Emeritus Professor Michael Hensley, Ms Jenny Mackney
Scheme Equipment Grant
Role Investigator
Funding Start 2012
Funding Finish 2012
GNo G1100973
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

Phenotype based management of severe persistent asthma$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Vanessa McDonald, Doctor Katie Baines, Conjoint Professor Peter Gibson
Scheme Research Grant
Role Investigator
Funding Start 2012
Funding Finish 2012
GNo G1101169
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

Gene expression markers, mechanisms and steroid response of neutrophilic asthma$15,000

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Doctor Katie Baines
Scheme Fellowship Grant
Role Lead
Funding Start 2012
Funding Finish 2012
GNo G1200082
Type Of Funding Internal
Category INTE
UON Y

20117 grants / $92,989

Transcriptional Phenotyping of COPD and the relationship between neutrophilic airway inflammation, airway infection and activation of proinflammatory pathways$24,000

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Doctor Katie Baines, Conjoint Professor Peter Gibson, Professor Jodie Simpson
Scheme Research Grant
Role Lead
Funding Start 2011
Funding Finish 2011
GNo G1100635
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

Identification of a specific biomarker signature that identifies asthma phenotype $23,700

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Katie Baines, Professor Jodie Simpson, Conjoint Professor Peter Gibson
Scheme Project Grant
Role Lead
Funding Start 2011
Funding Finish 2011
GNo G1001054
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

Transcriptional Phenotyping of COPD and the relationship between neutrophilic airway inflammation, airway infection and activation of proinflammatory pathways$20,000

Funding body: Lung Foundation Australia

Funding body Lung Foundation Australia
Project Team Doctor Katie Baines
Scheme Grant-In-Aid for New and Emerging Researchers
Role Lead
Funding Start 2011
Funding Finish 2011
GNo G1000976
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Epigenetic changes in infants associated with maternal asthma during pregnancy$10,000

Funding body: Thoracic Society of Australia and New Zealand

Funding body Thoracic Society of Australia and New Zealand
Project Team Doctor Katie Baines
Scheme Grant-in-aid (supported by Merck Sharp & Dohme)
Role Lead
Funding Start 2011
Funding Finish 2011
GNo G1000991
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Lung Function (Spirometry) testing and sputum induction equipment - establishing 3 new clinical workstations. Medgraphics CPFS/d USB spirometer with breezesuite software (x3). Laptop computer (x3). Ul$10,000

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Conjoint Professor Peter Gibson, Professor Jodie Simpson, Professor Lisa Wood, Doctor Katie Baines, Conjoint Professor Peter Wark, Doctor Vanessa Murphy
Scheme Equipment Grant
Role Investigator
Funding Start 2011
Funding Finish 2011
GNo G1100038
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

PULSE Education Prize$4,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Katie Baines
Scheme PULSE Education Prize
Role Lead
Funding Start 2011
Funding Finish 2011
GNo G1100342
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

Thoracic Society of Australia and New Zealand, Perth Convention and Exhibition Centre, 2 - 6 April 2011$1,289

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

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Katie Baines
Scheme Travel Grant
Role Lead
Funding Start 2011
Funding Finish 2011
GNo G1100297
Type Of Funding Internal
Category INTE
UON Y

20101 grants / $34,000

Real time PCR machine (Mastercycler ep realplex2 from Epprndorf) $34,000

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Jodie Simpson, Conjoint Professor Peter Gibson, Conjoint Professor Peter Wark, Professor Lisa Wood, Doctor Vanessa Murphy, Doctor Robert Scott, Doctor Katie Baines
Scheme Equipment Grant
Role Investigator
Funding Start 2010
Funding Finish 2010
GNo G1000056
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

20091 grants / $63,354

Epigenetic regulation of airways inflammation in non-eosinophilic asthma$63,354

Funding body: Asthma Foundation of New South Wales

Funding body Asthma Foundation of New South Wales
Project Team Conjoint Professor Peter Gibson, Doctor Katie Baines, Professor Jodie Simpson
Scheme PhD Scholarships
Role Investigator
Funding Start 2009
Funding Finish 2011
GNo G0189748
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20083 grants / $311,655

Molecular mechanisms and treatment of non-eosinophilic asthma$300,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Jodie Simpson, Doctor Katie Baines
Scheme Project Grant
Role Investigator
Funding Start 2008
Funding Finish 2010
GNo G0188825
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

Molecular subtypes of asthma defined by gene expression profiling$9,955

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Doctor Katie Baines
Scheme Early Career Researcher Grant
Role Lead
Funding Start 2008
Funding Finish 2008
GNo G0189618
Type Of Funding Internal
Category INTE
UON Y

American Thoracic Society, Metro Toronto Convention Centre, 16/5/2008 - 21/5/2008$1,700

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Doctor Katie Baines
Scheme Travel Grant
Role Lead
Funding Start 2008
Funding Finish 2008
GNo G0188599
Type Of Funding Internal
Category INTE
UON Y

20061 grants / $18,837

Molecular Pathogenesis of Non-Eosinophilic Asthma$18,837

Funding body: Asthma Foundation of New South Wales

Funding body Asthma Foundation of New South Wales
Project Team Doctor Katie Baines, Conjoint Professor Peter Gibson
Scheme PhD Scholarships
Role Lead
Funding Start 2006
Funding Finish 2006
GNo G0185985
Type Of Funding Donation - Aust Non Government
Category 3AFD
UON Y

20041 grants / $37,837

Molecular Pathogensis of Non-Eosinphilic Asthma$37,837

Funding body: Asthma Foundation of New South Wales

Funding body Asthma Foundation of New South Wales
Project Team Conjoint Professor Peter Gibson, Laureate Professor Rodney Scott, Doctor Katie Baines
Scheme PhD Scholarships
Role Investigator
Funding Start 2004
Funding Finish 2005
GNo G0183715
Type Of Funding Donation - Aust Non Government
Category 3AFD
UON Y

1 grants / $20,000

Gene expression profiling – a novel and efficient method for phenotyping severe asthma? $20,000

Funding body: National Clinical CRE in Severe Asthma

Funding body National Clinical CRE in Severe Asthma
Project Team Mr Marcus Christensen, Doctor Katie Baines
Scheme Seed Research Project
Role Lead
Funding Start
Funding Finish
GNo G1700752
Type Of Funding Internal
Category INTE
UON Y
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Research Supervision

Number of supervisions

Completed3
Current7

Total current UON EFTSL

PhD1.5

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2017 PhD Investigating Aberrant Inflammatory Signaling in Asthma PhD (Medicine), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2016 PhD Dietary Fibre As A Modulator of Inflammation In Asthma PhD (Nutritional Biochemistry), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2016 PhD Fruit and Vegetable Extract for the Reduction of Obesity-Induced Inflammation PhD (Nutritional Biochemistry), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2015 PhD The effects of Galectin-3 on alveolar macrophage function in asthma PhD (Medicine), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2015 PhD Characterization of neutrophil subtypes in obstructive airway disease. PhD (Medicine), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2015 PhD The Relationship Between Blood Eosinophilia, Exhaled Nitric Oxide and Airflow Obstruction in Asthma and COPD Patients from the Community of Busselton, Australia PhD (Medicine), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2015 PhD Inflammatory gene expression profiling during pregnancy to predict future asthma exacerbations and poor maternal and neonatal outcomes PhD (Reproductive Medicine), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor

Past Supervision

Year Level of Study Research Title Program Supervisor Type
2017 PhD The Role of Comorbidities and Inflammation in COPD PhD (Medicine), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2017 PhD Fatty Acids and the Innate Immune Response PhD (Nutritional Biochemistry), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2014 PhD Epigenetic Regulation of Airway Inflammation in Asthma PhD (Medicine), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
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News

NHMRC

NHMRC funding success 2016

November 13, 2015

Dr Katie Baines has been awarded more than $585,000 in NHMRC Project Grant funding commencing in 2016 for her research project Targeting neutrophil extracellular traps to reduce inflammation in severe asthma.

New study to examine fibre effect on asthma

June 15, 2015

Respiratory researchers from the University of Newcastle and HMRI are looking into whether a high-fibre diet can reduce airway inflammation in people with asthma.

Associate Professor Lisa Wood

Fruit-and-veg capsule set to combat obesity impacts

March 24, 2014

Hunter Medical Research Institute researchers are examining whether a simple fruit-and-vegetable supplement, taken in capsule form, can reduce inflammation produced by fat cells and thereby lower the risk of heart disease, diabetes, asthma and cancers in overweight people.

Dr Katie Baines

Position

Post-Doctoral Research Fellow
Respiratory Medicine
School of Medicine and Public Health
Faculty of Health and Medicine

Contact Details

Email katherine.baines@newcastle.edu.au
Phone (02) 40420090
Fax (02) 40420046

Office

Room Room 2109 Level 2 West Wing
Building Hunter Medical Research Institute
Location HMRI Building

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