Dr Adam Collison

Dr Adam Collison

Lecturer

School of Medicine and Public Health (Public Health)

An insight into immunology and allergic responses

An early fascination with immunology has led to an already highly-awarded career with a focus on identifying and treating allergies.

Dr Adam Collison

Dr Adam Collison’s research explores why some people develop allergies, while others, who are exposed to the same triggers don’t. His work is focussed on the exposures that occur in the first years of life, including in-utero. “I’m interested in why and how we become allergic - and if that can be prevented,” Adam explains.

Since being awarded his PhD from UON in 2012, Adam has received multiple awards for his research, including the University of Newcastle Priority Research Centre for Asthma and Respiratory Disease early career award.

With an intense focus on allergic responses, Adam has honed his research focus to explore three specific areas of immunology.

“In particular, I’m looking at asthma, food allergy and a rarer disease; Eoinophilic Oesophagitis, which is an inflamed foodpipe,” Adam says.

As his background is in immunology, Adam’s research also hones in on the interaction between the immune system and environmental bacteria and viruses in the lung and in the gut and the interplay between the two.  “One of the roles of the immune system is to watch out for potential infections; the different components that are unique to bacteria and virus are constantly being watched for. The number and type of these signals is then interpreted by the immune system and it chooses which white blood cells and antibacterial / antiviral compounds to release in response. These responses also often involve significant collateral damage to the host,” Adam explains.

Another focus is the difference species of bacteria in the gut which digest different foods in different ways “Much of the by-products of these processes are absorbed by the host as nutrients which have been shown to have implications in a broad range of health issues from asthma to depression to obesity,” Adam says.

From whales to well-being

It’s not always a direct path to research. Growing up Adam wanted to be a Marine Biologist, “But when I was in about Year 8  I started to think about life more deeply and realised that I’d rather do something that has more direct impact to help people. So medical research was a way to focus on people’s well-being while still doing something interesting.”

“Throughout High School I did reading in that kind of space and immunology particularly intrigued me. What I liked about the field that it was one of the least well-understood areas of health: we’re only really beginning to understand it. So when you combine that with the ability to really make a difference in people’s lives that made the decision simple,” Adam says.

Adam studied biomedical science at UON, then honours and a PhD in the same group he’s working with at HMRI now. “While I was doing my undergrad there were a few researchers who moved to Newcastle and it became one of the best places in Australia to do asthma research. We have a vibrant asthma research community here with great opportunities to do immunology research and that’s why I’ve hung around. Good opportunities, good mentoring and it’s a good spot to live too,” Adam says with a smile.

Better diagnosis of food allergies

Food allergy impacts one in 20 children and around two in 100 adults in Australia. While many allergies are mild, some can be severe and life-threatening. Currently, for clinicians to diagnose allergy people will undergo a skinprick test which can confirm or exclude allergic triggers. However, there are a range of people who aren’t necessarily allergic, but are sensitised to an allergen – and current tests can’t reveal the severity of an allergy.

Adam and his team are currently developing a blood test to better diagnose food allergies. “We’ve found a blood test that can not only tell us who’s allergic and who’s not allergic, but it’s the first test that can show who will have a severe anaphylactic reaction, and who will have a milder allergic reaction as well. We’ve proved it in our first population of study and we’re currently working on proving it in our second population,” Adam notes.

“Our ultimate aim is that this blood test will take the place of the challenge tests, but it may just be another tool.”

Breathing easier

During his honours work Adam discovered a new pathway that’s responsible for asthma. The work used genetically modified mice in asthma models to allow them to see how the asthma was different in the absence of TNF-related apoptosis-inducing ligand (TRAIL) signalling. “At this point TRAIL had been well described for its role in inducing apoptosis, which is a form of suicide for cells that have started to become cancerous, but its role in regulating inflammatory diseases such as asthma had been poorly described. We were able to conduct microarrays to quantify the expression of all known genes in asthmatic mice and found targets that were different between normal mice, which develop asthma in these models, and the genetically modified mice, which were protected.”

This was the first time these pathways had been associated with asthma. “We were able to confirm that these pathways were also dysregulated in human disease. We were then able to selectively target these downstream signalling pathways and demonstrate we were able to protect from asthma in the mouse models,” Adam explains.

Outreach to inspire our future scientists

Adam grew up in a country town, with very few researchers to inspire him, so he’s determined to encourage a new generation to think big. “Even though we live in Newcastle which has a large scientific community – many people around here that I meet socially are oblivious the research that’s being done. I think people should know what we’re doing here – because what we do, we do very well,” Adam says.

Grabbing the attention of students when they’re young, curious and interested is the aim of science outreach, and something that Adam is keen on. “I’m particularly interested in trying to communicate that to high school students and younger. When I was an undergrad I had the opportunity to work in the SMART program where you go around and talk to kids in Primary School in a fun way to create and foster that interest,” Adam enthuses.

Adam is also an early career researcher within the Priority Research Centre Grow Up Well. “All of my work really fits under this banner,” Adam explains of the PRC which Is focussed on improving child health and generating measurable health impacts for communities.  “One of my roles in this PRC is community engagement, so I have coordinated a community forum for National Science Week including lab tours, seminars and a forum where a panel answered questions from the community.  This is just the start of our community engagement - we intend to run similar sessions quarterly,” explains Adam.

“The PRC also provides an excellent opportunity for me to collaborate with researchers who have complimentary interests and work with clinicians to target unmet clinical needs for kids here in Newcastle that are also translatable more broadly to Australia and the world,” Adam adds.

“As researchers we’re very privileged to have the opportunity to pursue these things, with public support and government funding. So with that privilege comes the desire to do things to help as many people as possible,” Adam concludes.

An insight into immunology and allergic responses

Dr Adam Collison’s research explores why some people develop allergies, while others, who are exposed to the same triggers don’t.

Read more

Career Summary

Biography

To be a healthy adult, you need to grow up well in early life. Most chronic diseases that influence adult quality of life and life expectancy begin in childhood, thus, prevention and early intervention are key to reducing their impact.

Allergy is the fastest growing chronic disease in Australia affecting around 4.1 million people. While asthma has been recognised as a national health priority since 1999, there is increasing interest in food allergy, with as many as one in ten Australian infants testing positive to a food allergy. Alarmingly, the rate of hospital admissions for anaphylaxis has increased fourfold over the past 25 years. Food allergy associated diseases such as Eosinophilic Oesophagitis (a chronic condition of an inflamed food pipe) have also been increasing over the past two decades.

My vision is to undertake cutting-edge research in close collaboration with other world-leading scientists and medical doctors, to develop better diagnostics and treatments for these common and debilitating diseases. We need to address the urgent need to better understand the development of asthma and allergy in early life, so as to deliver lifelong better health outcomes to the growing number of Australians impacted by these chronic diseases.

My research has focused upon identification of novel therapeutic targets and molecular biomarkers to assist in better identification and treatment of asthma and food allergy in order to address currently unmet clinical needs. I have identified a novel proinflammatory signalling pathway downstream of tumour necrosis factor apoptosis inducing ligand (TRAIL) that is dysregulated in human asthmatics and eosinophilc oesophagitis patients. I have effectively targeted this pathway to therapeutic benefit in mouse models of rhinovirus induced allergic airways exacerbation – the current cause of over 80% of childhood asthma attacks presenting to hospital. This patent was licensed to Israeli based drug development company Proteologics in 2013. 

I have a particular interest in the epigenetic regulation of asthma, and have modulated miRNA to therapeutic benefit in vivo using mouse models of allergic airways disease. 

I have identified and patented a novel biomarker that in early studies enables stratification of peanut allergy severity, and allows accurate prediction of anaphylaxis risk upon subsequent food challenge. This is the first test in the world to measure food allergy severity and has the potential to radically modify the management of peanut allergy. 

Qualifications

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

Keywords

  • Allergy
  • Asthma
  • Eosinophilic Oesophagitis
  • Food Allergy
  • Immunology
  • Microbiology
  • Paediatrics

Fields of Research

Code Description Percentage
060699 Physiology not elsewhere classified 25
110799 Immunology not elsewhere classified 75

Professional Experience

UON Appointment

Title Organisation / Department
Lecturer University of Newcastle
School of Medicine and Public Health
Australia

Awards

Research Award

Year Award
2016 PRC GrowUpWell EMCR Travel Award
PRC GrowUpWell
2015 PRC Asthma and Respiratory Disease Early Career Researcher Award
Priority Research Centre for Asthma and Respiratory Disease
2012 CRC Asthma International Travel Award
Unknown
2011 HCRF Achievement in Research Award
Unknown
2010 ASI International Travel Award
Unknown
2010 ASI National Travel Award
Unknown
2010 Newcastle Innovation Student Excellence Award
Newcastle Innovation
2010 AusBiotech / Glaxo Smith Kline Student Excellence Award
AusBiotech / Glaxo Smith Kline
2009 ASI NSW presentation award
Unknown
2008 Best Presentation University of Newcastle Research Showcase
University of Newcastle
2007 Asthma CRC PhD top-up
Unknown

Patents

Number Title Patent Family Registered Approved
13/885,491 Signal transduction pathway modulation
Provided herein are methods and compositions for modulating signal transduction pathways 
by regulating the expression and/or activity of Midline-1, enabling the inhibition of airways 
inflammation, the inhibition of airways hyperresponsiveness, the inhibition of rhinovirus-
associated inflammation, and reductions in cytokine and chemokine release. Methods and 
compositions disclosed herein facilitate the treatment and prevention of conditions 
associated with airway inflammation, airway tissue remodelling and rhinovirus-associated ...
US 15/11/2010 2011
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Publications

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


Journal article (30 outputs)

Year Citation Altmetrics Link
2017 Kepreotes E, Whitehead B, Attia J, Oldmeadow C, Collison A, Searles A, et al., 'High-flow warm humidified oxygen versus standard low-flow nasal cannula oxygen for moderate bronchiolitis (HFWHO RCT): an open, phase 4, randomised controlled trial', The Lancet, 389 930-939 (2017)

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

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

DOI 10.1016/S0140-6736(17)30061-2
Citations Web of Science - 1
Co-authors Joerg Mattes, John Attia, Christopher Oldmeadow
2017 Foster PS, Maltby S, Rosenberg HF, Tay HL, Hogan SP, Collison AM, et al., 'Modeling TH 2 responses and airway inflammation to understand fundamental mechanisms regulating the pathogenesis of asthma.', Immunol Rev, 278 20-40 (2017)
DOI 10.1111/imr.12549
Citations Scopus - 2Web of Science - 1
Co-authors Steven Maltby, Ming Yang, Philip Hansbro, Paul Foster, Joerg Mattes
2017 Girkin JL, Hatchwell LM, Collison AM, Starkey MR, Hansbro PM, Yagita H, et al., 'TRAIL signaling is proinflammatory and proviral in a murine model of rhinovirus 1B infection', American Journal of Physiology - Lung Cellular and Molecular Physiology, 312 L89-L99 (2017)

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

© 2017 the American Physiological Society. The aim of this study is to elucidate the role of TRAIL during rhinovirus (RV) infection in vivo. Naïve wild-type and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-deficient (Tnfsf10 -/- ) BALB/c mice were infected intranasally with RV1B. In separate experiments, Tnfsf10 -/- mice were sensitized and challenged via the airway route with house dust mite (HDM) to induce allergic airways disease and then challenged with RVIB or UV-RVIB. Airway hyperreactivity (AHR) was invasively assessed as total airways resistance in response to increasing methacholine challenge and inflammation was assessed in bronchoalveolar lavage fluid at multiple time points postinfection. Chemokines were quantified by ELISA of whole lung lysates and viral load was determined by quantitative RT-PCR and tissue culture infective dose (TCID 50 ). Human airway epithelial cells (BEAS2B) were infected with RV1B and stimulated with recombinant TRAIL or neutralizing anti-TRAIL antibodies and viral titer assessed by TCID50. HDM-challenged Tnfsf10 -/- mice were protected against RV-induced AHR and had suppressed cellular infiltration in the airways upon RV infection. Chemokine C-X-C-motif ligand 2 (CXCL2) production was suppressed in naïve Tnfsf10 -/- mice infected with RV1B, with less RV1B detected 24 h postinfection. This was associated with reduced apoptotic cell death and a reduction of interferon (IFN)-¿2/3 but not IFN-a or IFN-ß. TRAIL stimulation increased, whereas anti-TRAIL antibodies reduced viral replication in RV1B-infected BEAS2B cells in vitro. In conclusion, TRAIL promotes RV-induced AHR, inflammation and RV1B replication, implicating this molecule and its downstream signaling pathways as a possible target for the amelioration of RV1B-induced allergic and nonallergic lung inflammation and AHR.

DOI 10.1152/ajplung.00200.2016
Citations Scopus - 1Web of Science - 1
Co-authors Paul Foster, Joerg Mattes, Malcolm Starkey, Philip Hansbro
2017 Dunn A, Pearce K, Callister R, Collison A, Morten M, Mandaliya P, et al., 'Exercise capacity is not decreased in children who have undergone lung resection early in life for congenital thoracic malformations compared to healthy age-matched children.', Pediatr Pulmonol, (2017)
DOI 10.1002/ppul.23772
Co-authors Robin Callister, Joerg Mattes
2016 Sokulsky LA, Collison AM, Nightingale S, Le Fevre A, Percival E, Starkey MR, et al., 'TRAIL deficiency and PP2A activation with salmeterol ameliorates egg allergen-driven eosinophilic esophagitis', American Journal of Physiology - Gastrointestinal and Liver Physiology, 311 G998-G1008 (2016) [C1]

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

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

DOI 10.1152/ajpgi.00151.2016
Citations Scopus - 1Web of Science - 1
Co-authors Malcolm Starkey, Joerg Mattes, Paul Foster, Philip Hansbro
2016 Haw TJ, Starkey MR, Nair PM, Pavlidis S, Liu G, Nguyen DH, et al., 'A pathogenic role for tumor necrosis factor-related apoptosis-inducing ligand in chronic obstructive pulmonary disease', Mucosal Immunology, 9 859-872 (2016) [C1]

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

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

DOI 10.1038/mi.2015.111
Citations Scopus - 9Web of Science - 13
Co-authors Jay Horvat, Philip Hansbro, Alan Hsu, Peter Wark, Darryl Knight, Joerg Mattes, Paul Foster, Malcolm Starkey
2016 Maltby S, Plank M, Tay HL, Collison A, Foster PS, 'Targeting MicroRNA function in respiratory diseases: Mini-review', Frontiers in Physiology, 7 (2016) [C1]
DOI 10.3389/fphys.2016.00021
Citations Scopus - 15Web of Science - 11
Co-authors Hock Tay, Steven Maltby, Paul Foster
2016 Judd LM, Heine RG, Menheniott TR, Buzzelli J, O Brien-Simpson N, Pavlic D, et al., 'Elevated IL-33 expression is associated with pediatric eosinophilic esophagitis, and exogenous IL-33 promotes eosinophilic esophagitis development in mice', American Journal of Physiology - Gastrointestinal and Liver Physiology, 310 G13-G25 (2016) [C1]

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

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

DOI 10.1152/ajpgi.00290.2015
Citations Scopus - 8Web of Science - 7
Co-authors Joerg Mattes
2016 Percival E, Bhatia R, Preece K, McElduff P, McEvoy M, Collison A, Mattes J, 'Reproducibility of serum IgE, Ara h2 skin prick testing and fraction of exhaled nitric oxide for predicting clinical peanut allergy in children', ALLERGY ASTHMA AND CLINICAL IMMUNOLOGY, 12 (2016) [C1]
DOI 10.1186/s13223-016-0143-z
Co-authors Mark Mcevoy, Patrick Mcelduff, Joerg Mattes
2015 Collison AM, Sokulsky LA, Sherrill JD, Nightingale S, Hatchwell L, Talley NJ, et al., 'TNF-related apoptosis-inducing ligand (TRAIL) regulates midline-1, thymic stromal lymphopoietin, inflammation, and remodeling in experimental eosinophilic esophagitis', Journal of Allergy and Clinical Immunology, 136 971-982 (2015) [C1]

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

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

DOI 10.1016/j.jaci.2015.03.031
Citations Scopus - 4Web of Science - 3
Co-authors Marjorie Walker, Nicholas Talley, Joerg Mattes
2015 Schilter HC, Collison A, Russo RC, Foot JS, Yow TT, Vieira AT, et al., 'Effects of an anti-inflammatory VAP-1/SSAO inhibitor, PXS-4728A, on pulmonary neutrophil migration', Respiratory Research, 16 (2015) [C1]

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

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

DOI 10.1186/s12931-015-0200-z
Citations Scopus - 9Web of Science - 11
Co-authors Joerg Mattes
2015 Hatchwell L, Collison A, Girkin J, Parsons K, Li J, Zhang J, et al., 'Toll-like receptor 7 governs interferon and inflammatory responses to rhinovirus and is suppressed by IL-5-induced lung eosinophilia', Thorax, (2015) [C1]

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

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

DOI 10.1136/thoraxjnl-2014-205465
Citations Scopus - 21Web of Science - 19
Co-authors Nathan Bartlett, Paul Foster, Joerg Mattes, Darryl Knight, Peter Wark
2015 Girkin J, Hatchwell L, Foster P, Johnston SL, Bartlett N, Collison A, Mattes J, 'CCL7 and IRF-7 mediate hallmark inflammatory and IFN responses following rhinovirus 1B infection', Journal of Immunology, 194 4924-4930 (2015) [C1]

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

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

DOI 10.4049/jimmunol.1401362
Citations Scopus - 9Web of Science - 9
Co-authors Nathan Bartlett, Joerg Mattes, Paul Foster
2014 Starkey MR, Nguyen DH, Essilfie AT, Kim RY, Hatchwell LM, Collison AM, et al., 'Tumor necrosis factor-related apoptosis-inducing ligand translates neonatal respiratory infection into chronic lung disease.', Mucosal Immunol, 7 478-488 (2014) [C1]
DOI 10.1038/mi.2013.65
Citations Scopus - 14Web of Science - 14
Co-authors Paul Foster, Joerg Mattes, Jay Horvat, Malcolm Starkey, Philip Hansbro
2014 Hatchwell L, Girkin J, Morten M, Collison A, Mattes J, Foster PS, et al., 'Salmeterol attenuates chemotactic responses in rhinovirus-induced exacerbation of allergic airways disease¿by modulating protein phosphatase 2A', Journal of Allergy and Clinical Immunology, (2014) [C1]

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

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

DOI 10.1016/j.jaci.2013.11.014
Citations Scopus - 18Web of Science - 16
Co-authors Joerg Mattes, Paul Foster, Matt Dun, Nikki Verrills
2014 Tay HL, Plank M, Collison A, Mattes J, Kumar RK, Foster PS, 'MicroRNA: Potential biomarkers and therapeutic targets for allergic asthma?', Annals of Medicine, 46 633-639 (2014) [C1]

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

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

DOI 10.3109/07853890.2014.958196
Citations Scopus - 11Web of Science - 11
Co-authors Hock Tay, Paul Foster, Joerg Mattes
2014 Preece K, Bhatia R, Belcher J, Patchett K, McElduff P, Collison A, Mattes J, 'The fraction of exhaled nitric oxide improves prediction of clinical allergic reaction to peanut challenge in children', CLINICAL AND EXPERIMENTAL ALLERGY, 44 371-380 (2014) [C1]
DOI 10.1111/cea.12258
Citations Scopus - 3Web of Science - 4
Co-authors Patrick Mcelduff, Joerg Mattes
2014 Collison A, Li J, Pereira De Siqueira A, Zhang J, Toop HD, Morris JC, et al., 'Tumor necrosis factor-related apoptosis-inducing ligand regulates hallmark features of airways remodeling in allergic airways disease', American Journal of Respiratory Cell and Molecular Biology, 51 86-93 (2014) [C1]

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

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

DOI 10.1165/rcmb.2013-0490OC
Citations Scopus - 15Web of Science - 15
Co-authors Paul Foster, Joerg Mattes
2013 de Souza Alves CC, Collison A, Hatchwell L, Plank M, Morten M, Foster PS, et al., 'Inhibiting AKT phosphorylation employing non-cytotoxic anthraquinones ameliorates TH2 mediated allergic airways disease and rhinovirus exacerbation.', PLoS One, 8 e79565 (2013) [C1]
DOI 10.1371/journal.pone.0079565
Citations Scopus - 12Web of Science - 10
Co-authors Paul Foster, Joerg Mattes
2013 Foster PS, Plank MW, Collison AM, Tay HL, Kaiko GE, Li J, et al., 'The emerging role of microRNAs in regulating immune and inflammatory responses in the lung', Immunological Reviews, 253 198-215 (2013) [C1]
Citations Scopus - 40Web of Science - 40
Co-authors Philip Hansbro, Hock Tay, Ming Yang, Joerg Mattes, Paul Foster
2013 Barry J, Loh Z, Collison A, Mazzone S, Lalwani A, Zhang V, et al., 'Absence of Toll-IL-1 Receptor 8/Single Immunoglobulin IL-1 Receptor-Related Molecule Reduces House Dust Mite-Induced Allergic Airway Inflammation in Mice', AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 49 481-490 (2013) [C1]
DOI 10.1165/rcmb.2012-0425OC
Citations Scopus - 10Web of Science - 10
Co-authors Paul Foster, Joerg Mattes
2013 Collison AM, Hatchwell LM, Verrills NM, Wark PA, Pereira De Siqueira AL, Tooze MK, et al., 'The E3 ubiquitin ligase midline 1 promotes allergen and rhinovirus-induced asthma by inhibiting protein phosphatase 2A activity', Nature Medicine, 19 232-237 (2013) [C1]
Citations Scopus - 65Web of Science - 61
Co-authors Peter Wark, Nikki Verrills, Paul Foster, Nathan Bartlett, Joerg Mattes
2013 Collison A, Siegle JS, Hansbro NG, Kwok C-T, Herbert C, Mattes J, et al., 'Epigenetic changes associated with disease progression in a mouse model of childhood allergic asthma', DISEASE MODELS & MECHANISMS, 6 993-1000 (2013) [C1]
DOI 10.1242/dmm.011247
Citations Scopus - 9Web of Science - 8
Co-authors Joerg Mattes, Nicole Hansbro, Paul Foster
2011 Collison AM, Herbert C, Siegle JS, Mattes J, Foster PS, Kumar RK, 'Altered expression of microRNA in the airway wall in chronic asthma: miR-126 as a potential therapeutic target', BMC Pulmonary Medicine, 11 29 (2011) [C1]
Citations Scopus - 68Web of Science - 60
Co-authors Joerg Mattes, Paul Foster
2011 Collison AM, Mattes J, Plank MW, Foster PS, 'Inhibition of house dust mite-induced allergic airways disease by antagonism of microRNA-145 is comparable to glucocorticoid treatment', Journal of Allergy and Clinical Immunology, 128 160-U251 (2011) [C1]
Citations Scopus - 114Web of Science - 93
Co-authors Paul Foster, Joerg Mattes
2009 Mattes J, Collison AM, Plank MW, Phipps S, Foster PS, 'Antagonism of microRNA-126 suppresses the effector function of T(H)2 cells and the development of allergic airways disease', Proceedings of the National Academy of Sciences of the United States of America, 106 18704-18709 (2009) [C1]
DOI 10.1073/pnas.0905063106
Citations Scopus - 237Web of Science - 211
Co-authors Joerg Mattes, Paul Foster
2009 Collison AM, Foster PS, Mattes J, 'Emerging role of tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) as a key regulator of inflammatory responses', Clinical and Experimental Pharmacology and Physiology, 36 1049-1053 (2009) [C1]
DOI 10.1111/j.1440-1681.2009.05258.x
Citations Scopus - 37Web of Science - 37
Co-authors Paul Foster, Joerg Mattes
2009 Phipps S, Lam CE, Kaiko GE, Foo A, Collison AM, Mattes J, et al., 'Toll/IL-1 signaling is critical for house dust mite-specific Th1 and Th2 responses', American Journal of Respiratory and Critical Care Medicine, 179 883-893 (2009) [C1]
DOI 10.1164/rccm.200806-974oc
Citations Scopus - 115Web of Science - 111
Co-authors Paul Foster, Joerg Mattes
2008 Mattes J, Collison AM, Foster PS, 'Emerging role of microRNAs in disease pathogenesis and strategies for therapeutic modulation', Current Opinion in Molecular Therapeutics, 10 150-157 (2008) [C1]
Citations Scopus - 42Web of Science - 37
Co-authors Paul Foster, Joerg Mattes
2007 Weckmann M, Collison A, Simpson JL, Kopp MV, Wark PA, Smyth MJ, et al., 'Critical link between TRAIL and CCL20 for the activation of T(H)2 cells and the expression of allergic airway disease', Nature Medicine, 13 1308-1315 (2007) [C1]
DOI 10.1038/nm1660
Citations Scopus - 80Web of Science - 76
Co-authors Peter Gibson, Peter Wark, Paul Foster, Jodie Simpson, Joerg Mattes, Nicole Hansbro
Show 27 more journal articles

Conference (27 outputs)

Year Citation Altmetrics Link
2017 Morten M, Collison A, Murphy V, Barker D, Meredith J, Powell H, et al., 'ASTHMA CONTROL DURING PREGNANCY, 17Q21 VARIANTS AND CHILDHOOD-ONSET ASTHMA', RESPIROLOGY (2017)
Co-authors Vanessa Murphy, Joerg Mattes, Peter Gibson
2017 Collison A, Li J, De Siqueira AP, Lv X, Toop HD, Morris JC, et al., 'THE E3 UBIQUITIN LIGASE MID1 PROMOTES IDIOPATHIC PULMONARY FIBROSIS', RESPIROLOGY (2017)
Co-authors Philip Hansbro, Joerg Mattes, Malcolm Starkey
2016 Kepreotes E, Whitehead B, Lee M, Collison A, Goddard B, Cheese L, et al., 'HIGH-FLOW OXYGEN COMPARED TO STANDARD NASAL CANNULA OXYGEN DOES NOT REDUCE THE MEDIAN TIME ON OXYGEN FOR INFANTS WITH MODERATE BRONCHIOLITIS', RESPIROLOGY (2016)
Co-authors Joerg Mattes, John Attia, Christopher Oldmeadow
2016 Collison A, Sokulsky LA, Starkey MR, Nightingale S, Le Fevre A, Percival E, et al., 'TRAIL regulates egg-allergen induced eosinophilic oesophagitis', EUROPEAN JOURNAL OF IMMUNOLOGY (2016)
Co-authors Paul Foster, Joerg Mattes, Philip Hansbro, Malcolm Starkey
2015 Collison AM, Sokulsky LA, Sherrill JD, Nightingale S, Hatchwell L, Talley NJ, et al., 'TRAIL Signalling Is Pro-Inflammatory in Eosinophilic Esophagitis', JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY (2015) [E3]
Co-authors Joerg Mattes, Nicholas Talley, Marjorie Walker
2015 Hansbro P, Haw T, Nair P, Hanish I, Nguyen D, Liu G, et al., 'Tumour necrosis factor-related apoptosis inducing ligand promotes the development of experimental chronic obstructive pulmonary disease', JOURNAL OF IMMUNOLOGY (2015)
Co-authors Joerg Mattes, Darryl Knight, Philip Hansbro, Jay Horvat
2015 Percival E, Bhatia R, McElduff P, McEvoy M, Collison A, Mattes J, 'REPRODUCIBILITY OF ARA h2 SKIN PRICK TESTING AND FRACTION OF EXHALED NITRIC OXIDE IN THE ASSESSMENT OF PAEDIATRIC PEANUT ALLERGY', INTERNAL MEDICINE JOURNAL (2015) [E3]
Co-authors Mark Mcevoy, Patrick Mcelduff, Joerg Mattes
2014 Mandaliya PH, Bhatia R, Belcher J, McElduff P, Collison A, Mattes J, 'Is fraction of exhaled nitric oxide (FeNO) able to predict severity of allergic reaction at an open cooked egg challenge?', ALLERGY (2014) [E3]
Co-authors Patrick Mcelduff, Joerg Mattes
2014 Collison A, Hatchwell L, Girkin J, Parsons K, Li J, Zhang J, et al., 'Late-breaking abstract: IL-5-induced airways eosinophilia as a negative regulator of TLR7 expression may impair the interferon response to rhinovirus in allergic airways', EUROPEAN RESPIRATORY JOURNAL (2014)
Co-authors Joerg Mattes, Nathan Bartlett, Peter Wark, Paul Foster
2014 Collison A, Hatchwell L, Girkin J, Li J, Parsons K, Bartlett N, et al., 'REDUCED TLR7 EXPRESSION MAY UNDERPIN IMPAIRED RESPONSE TO VIRAL INFECTION IN ASTHMA', RESPIROLOGY (2014) [E3]
DOI 10.1111/resp.12263_5
Co-authors Joerg Mattes, Paul Foster, Peter Wark
2014 Li J, Collison A, De Siqueira PA, Zhang J, Mattes J, 'TUMOUR NECROSIS FACTOR RELATED APOPTOSIS INDUCING LIGAND (TRAIL) REGULATION OF PROTEIN PHOSPHATASE (PP)2A IS CRUCIAL FOR THE DEVELOPMENT OF BLEOMYCIN INDUCED PULMONARY FIBROSIS IN MICE', RESPIROLOGY (2014) [E3]
Co-authors Joerg Mattes
2014 Preece K, Bhatia R, Belcher J, Patchett K, Mcelduff P, Collison A, Mattes J, 'FRACTION OF EXHALED NITRIC OXIDE IS A NOVEL NON-INVASIVE PREDICTOR OF PEANUT ALLERGY', RESPIROLOGY (2014) [E3]
Co-authors Patrick Mcelduff, Joerg Mattes
2014 Girkin J, Sokulsky L, Hatchwell L, Starkey M, Collison A, Hansbro P, Mattes J, 'IDENTIFICATION OF A NOVEL INTERLEUKIN-13 SIGNALLING PATHWAY', RESPIROLOGY (2014) [E3]
Co-authors Joerg Mattes, Malcolm Starkey, Philip Hansbro
2013 Kumar RK, Collison A, Siegle JS, Hansbro NG, Kwok C-T, Herbert C, et al., 'Epigenetic Changes Associated With Disease Progression In A Model Of Childhood Allergic Asthma', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2013)
Co-authors Joerg Mattes, Paul Foster, Nicole Hansbro
2013 Girkin J, Hatchwell L, Foster PS, Johnston SL, Collison A, Mattes J, 'SALMETEROL ATTENUATES CHEMOTAXIS IN RHINOVIRUS-INDUCED EXACERBATION OF ASTHMA VIA MODULATION OF PP2A', RESPIROLOGY (2013) [E3]
Co-authors Joerg Mattes, Paul Foster
2013 Hatchwell L, Collison A, Phipps S, Foster PS, Johnston SL, Mattes J, 'CCL7 (MCP-3) MEDIATES RHINOVIRUS-INDUCED LUNG INFLAMMATION AND EXACERBATION OF ALLERGIC AIRWAY DISEASE', RESPIROLOGY (2013) [E3]
Co-authors Paul Foster, Joerg Mattes
2012 Collison AM, Hatchwell LM, Siqueira AP, Bartlett NW, Johnston SL, Foster PS, Mattes J, 'Antagonism of microRNA-122 is comparible to azithromycin treatment in a mouse model of rhinovirus-induced exacerbation of allergic airways disease', Respirology (2012) [E3]
Co-authors Paul Foster, Nathan Bartlett, Joerg Mattes
2012 Hatchwell LM, Collison AM, Siqueira AP, Bartlett NW, Johnston SL, Foster PS, Mattes J, 'Toll-like receptor 7 mediates anti-viral responses to rhinovirus while suppressing exacerbation of asthma', Respirology (2012) [E3]
Co-authors Paul Foster, Nathan Bartlett, Joerg Mattes
2012 Hatchwell LM, Collison AM, Siqueira AP, Bartlett NW, Johnston SL, Foster PS, Mattes J, 'TRAIL regulates inflammatory responses to rhinovirus and rhinovirus-induced exacerbation of asthma', Respirology (2012) [E3]
Co-authors Joerg Mattes, Paul Foster, Nathan Bartlett
2011 Collison AM, Hatchwell LM, Pereira De Siqueira AL, Don A, Verrills NM, Foster PS, Mattes J, 'The development of house dust mite-induced allergic airways disease is regulated by a novel E3 ubiquitin ligase-dependent deactivation of a protein phosphatase', Respirology (2011) [E3]
Co-authors Paul Foster, Nikki Verrills, Joerg Mattes
2011 Hatchwell LM, Collison AM, Pereira De Siqueira AL, Foster PS, Verrills NM, Don A, et al., 'A novel E3 ubiquitin ligase links rhinovirus infection to exacerbation of asthma', Respirology (2011) [E3]
Co-authors Peter Wark, Nikki Verrills, Joerg Mattes, Paul Foster
2011 Mattes J, Hankin RG, Hilton JM, Collison AM, Pereira De Siqueira AL, Gulliver T, et al., 'Frequent persistent wheeze in infancy may be associated with impaired FEV0.5 and FVC values', Respirology (2011) [E3]
Citations Web of Science - 1
Co-authors Paul Foster, Joerg Mattes
2010 Mattes J, Collison AM, Plank MW, Phipps S, Foster PS, 'The role of microRNA as new anti-inflammatory targets', APCAACI 2010: The 8th Asia Pacific Congress on Allergy, Asthma and Clinical Immunology Programme & Abstracts Handbook (2010) [E3]
Co-authors Paul Foster, Joerg Mattes
2010 Foster PS, Mattes J, Collison AM, Plank MW, Phipps S, 'MicoRNAs bridge innate and adative immunity: induction of TH2 mediated allergic airways disease', OzBio 2010: The Molecules of Life - from Discovery to Biotechnology. Abstracts (2010) [E3]
Co-authors Paul Foster, Joerg Mattes
2009 Collison AM, Mattes J, Phipps S, Plank MW, Foster PS, 'MicroRNAs are crucial in the development of airways hyperreactivity', American Journal of Respiratory and Critical Care Medicine (2009) [E3]
Co-authors Paul Foster, Joerg Mattes
2009 Mattes J, Collison AM, Plank MW, Phipps S, Foster PS, 'MicroRNAs regulate allergic airway inflammation', American Journal of Respiratory and Critical Care Medicine (2009) [E3]
Co-authors Paul Foster, Joerg Mattes
2009 Collison AM, De Siqueira A, Plank MW, Foster PS, Mattes J, 'The identification of TRAIL as a mediator of airways remodelling in a chronic model of murine allergic airways disease', American Journal of Respiratory and Critical Care Medicine (2009) [E3]
Co-authors Paul Foster, Joerg Mattes
Show 24 more conferences

Patent (1 outputs)

Year Citation Altmetrics Link
2013 Mattes J, Foster PS, Collison A, Hatchwell L, Signal transduction pathway modulation (2013)
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Grants and Funding

Summary

Number of grants 14
Total funding $1,317,757

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


20173 grants / $50,000

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

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Adam Collison, Professor Joerg Mattes
Scheme Project Grant
Role Lead
Funding Start 2017
Funding Finish 2017
GNo G1700818
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

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

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Joerg Mattes, Doctor Adam Collison
Scheme Commercialisation in Medical Research Grant
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1700816
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Countess II FL$10,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Malcolm Starkey, Doctor Adam Collison, Doctor Hock Tay, Doctor Aniruddh Deshpande, Mr Gang Liu, Doctor Jemma Mayall
Scheme Early and Mid-Career Equipment Grant
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1701221
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20156 grants / $1,195,886

The effect of asthma control during pregnancy on markers of airways inflammation and lung function in the offspring$1,102,896

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

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

A novel peanut allergy biomarker to predict anaphylaxis risk$29,942

Funding body: Thrasher Research Fund

Funding body Thrasher Research Fund
Project Team Doctor Adam Collison
Scheme Research Grant
Role Lead
Funding Start 2015
Funding Finish 2016
GNo G1500763
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

A novel diagnostic blood test for peanut allergy$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Adam Collison, Doctor Rani Bhatia
Scheme Research Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1500758
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

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

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Professor Joerg Mattes, Doctor Vanessa Murphy, Doctor Adam Collison
Scheme Research Grant
Role Investigator
Funding Start 2015
Funding Finish 2015
GNo G1500671
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

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

Funding body: Rebecca L Cooper Medical Research Foundation Ltd

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

American Academy of Asthma Allergin and Immunology, Houston USA, 20-23 Feb 2015$2,000

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

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Adam Collison
Scheme Travel Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1500340
Type Of Funding Internal
Category INTE
UON Y

20142 grants / $24,871

Miltenyi Biotec GentleMACS Octo Dissociator with Heaters $23,566

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

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

TSANZ Annual Meeting, Adelaide Australia, 4-9 April 2014$1,305

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

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Adam Collison
Scheme Travel Grant
Role Lead
Funding Start 2014
Funding Finish 2014
GNo G1400540
Type Of Funding Internal
Category INTE
UON Y

20131 grants / $25,000

The prediction of egg allergy severity in children by non-invasive exhaled nitric oxide (FeNO) measurement confirmed with food challenge.$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Adam Collison, Doctor Rani Bhatia
Scheme Research Grant
Role Lead
Funding Start 2013
Funding Finish 2013
GNo G1301150
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20122 grants / $22,000

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

Funding body: Hunter Medical Research Institute

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

American Thoracic Society annual meeting, San Dieago, 18 - 25 May 2012$2,000

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

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Adam Collison
Scheme Travel Grant
Role Lead
Funding Start 2012
Funding Finish 2012
GNo G1200605
Type Of Funding Internal
Category INTE
UON Y
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Research Supervision

Number of supervisions

Completed1
Current9

Total current UON EFTSL

PhD1.9

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2017 PhD Factors That May Influence The Development of Asthma and Other Respiratory Symptoms in Babies Born From Mothers Non-asthmatic PhD (Paediatrics), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2017 PhD Evaluation of the Effectiveness of a Comprehensive Smoking Cessation Intervention or Usual Care Before the Second Trimester of Pregnancy: A Randomised Controlled Trial in the Hunter region. PhD (Paediatrics), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2017 PhD The Role of Microbiome Development in the Early Origins of Asthma in a High-Risk Population PhD (Paediatrics), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2017 PhD The Impact of Better Asthma Management During Pregnancy on the Lung Function of the Child PhD (Paediatrics), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2016 PhD Risk factors for impaired lung function and the onset of respiratory disease in early life PhD (Paediatrics), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2016 PhD Dietary Intervention to Reduce Exacerbations in Children with Asthma PhD (Nutritional Biochemistry), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2015 PhD Food Allergy and Anaphylaxis Predictors PhD (Paediatrics), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2013 PhD Novel Approaches for the Management of Lung Disease in Children PhD (Paediatrics), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2012 PhD A Novel Role for the TRAIL Signalling Pathway in the Pathogenesis of Eosinophilic Oesophagitis PhD (Paediatrics), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor

Past Supervision

Year Level of Study Research Title Program Supervisor Type
2017 PhD The Role of Rhinovirus and Novel Molecular Mechanisms in Allergic Airways Disease PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
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Research Collaborations

The map is a representation of a researchers co-authorship with collaborators across the globe. The map displays the number of publications against a country, where there is at least one co-author based in that country. Data is sourced from the University of Newcastle research publication management system (NURO) and may not fully represent the authors complete body of work.

Country Count of Publications
Australia 51
United Kingdom 14
Japan 5
China 4
United States 4
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News

Dr Adam Collison

Asthma Researcher awarded TSANZ Career Development Fellowship

April 3, 2017

Dr Adam Collison has been awarded a TSANZ and National Asthma Council Asthma and Airways Career Development Fellowship to explore asthma in pregnancy.

Breakthrough in asthma research

March 27, 2017

Researchers from the University of Newcastle’s Healthy Lungs and Grow Up Well Priority Research Centres have reported on the results of a study which could effectively slash the rates of asthma in children of asthmatic mothers.

Triple treat for UON: Young Tall Poppies

September 29, 2016

Three innovative University Of Newcastle and HMRI researchers will be awarded the prestigious title of Young Tall Poppy in the science awards ceremony at the Museum of Applied Arts and Science on Thursday September 29, 2016.

Dr Adam Collison

Position

Lecturer
School of Medicine and Public Health
Faculty of Health and Medicine

Focus area

Public Health

Contact Details

Email adam.collison@newcastle.edu.au
Phone (02) 4042 0219

Office

Room HMRI level 2 East
Building HMRI Building
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