Dr Malcolm Starkey
Honorary Senior Lecturer
School of Biomedical Sciences and Pharmacy (Immunology and Microbiology)
- Email:malcolm.starkey@newcastle.edu.au
- Phone:(02) 40420204
An insight into the immune system
Dr Malcolm Starkey is focussed on how early-life infections can lead to long-term health issues.
Malcolm is an Australian Research Council (ARC) Discovery Early Career Research Award (DECRA) fellow at the Priority Research Centres for GrowUpWell and Healthy Lungs, based at the Hunter Medical Research Institute (HMRI). Previously a National Health and Medical Research Council (NHMRC) early career fellow, Malcolm’s research focusses on understanding how respiratory challenges in early life impair the development of the lungs and a healthy immune system.
Exploring how these respiratory challenges could predispose individuals to chronic diseases such as asthma and chronic obstructive pulmonary disease (COPD, more commonly known as emphysema), is a key focus of his work. However, Malcolm is also exploring how the immune system repairs the kidney after injury and is investigating strategies to prevent the development of chronic kidney disease.
An immunologist, Malcolm is using experimental models that seek to cement a mechanistic understanding of the early-life origins of chronic diseases. By using novel mouse models that recapitulate the hallmark features of human disease, his work has made important contributions and has led to the identification of novel therapeutic strategies that are under further investigations.
"It can be difficult to recruit humans, particularly young children, for clinical trials," Malcolm explains. "You need to have a strong rationale as to why you're going to do these studies. Our models provide pivotal preclinical evidence to justify this translational clinical work."
Malcolm’s research has already made a number of important contributions to the field of understanding severe asthma and emphysema. Straddling the microbiological and immunological fields, Malcolm's projects stress the "multifactorial" nature of several airway conditions. His work also emphasise the urgent need to identify the roles played by bacteria and viruses in the onset and progression of respiratory diseases.
"Using mouse models, we have learnt that severe respiratory infections in early life can trigger asthma and/or emphysema in adulthood," Malcolm says. "We've learnt that early life infections can cause irreparable damage to the lung, preventing normal healthy lung development and alter the way the immune system develops. It's really quite incredible."
Acutely aware of the lack of therapeutic options available for these chronic illnesses, Malcolm is hoping his research will be used to inform the development of new and innovative therapeutic strategies for patients.
"If we can't breathe, we can't function. We want people to breathe easy."
Of mice, men and molecules
Malcolm's research career began in 2008, when he undertook a PhD with Professor Phil Hansbro at the HMRI. Chiefly focussing on understanding the 'why' behind the 'what is,' the duo looked to figure out how infections predispose people to disease.
"There's emerging evidence that some chronic lung diseases such as asthma and emphysema may originate from infections – contracted either as a newborn or an infant."
Examining multiple molecular pathways, Malcolm sought to elucidate the effects of the transfer of Chlamydia from mother to baby during childbirth. "There is a cohort of neonates that are susceptible to this vertical transmission," he explains. “This is a vital stage because the lung is still developing. If the lung doesn't develop correctly, overall health can be negatively affected."
Going viral
Malcolm expanded upon this work after his PhD was conferred in early 2014, exploring the relationships between chronic airway diseases and infections. Concentrating research efforts on infections contracted in an early window post-birth, he is also studying the long-term effects of influenza, Streptococcus pneumoniae and nontypeable Haemophilus influenzae.
"Neonates are particularly vulnerable," he describes.
"The fetal immune system is altered in utero to prevent the mother's immune system rejecting the fetus during pregnancy," Malcolm says. "This contributes to an unbalanced and immature immune system in early life."
"If you happen to be unfortunate enough to contract a series of respiratory infections in early life, you are more likely to experience lung problems in the long term."
With recent clinical data showing some bacteria are important in this regard, Malcolm duly pursued this avenue of contemporary interest. "For some time it was thought that viruses cause this predisposition to asthma," he says. "As it turns out though, it probably doesn't matter whether it's viruses or bacteria – it can be both. It depends on many circumstances coming together, such as genetics, age of infection and the environment."
"We have found that early life infections cause the production of disease inducing factors. These factors promote long term effects by altering the immune system as well as the structure and function of the lung."
Malcolm's research has shown that therapies that target these factors may be effective new treatments for infection-induced chronic lung diseases.
Hypothesising that certain bacteria and viruses have an impact on the whole body, Malcolm and his team are after scientific proof of long-term systemic effects, such as changes in lung structure and development, and inappropriate immune system responses in the body.
Some of his more recent work has focused on viral exacerbations of chronic lung diseases. “Patients with chronic lungs diseases are more susceptible to the flu”. Malcolm and his colleagues and collaborators have discovered several novel mechanisms explaining why these patients are more susceptible to the flu.
Parts of a whole
Still dedicated to investigating the interplay between early life infections and acute airway conditions, Malcolm is working to address his evolving, specialist area from multiple angles and is aiming to examine links between these insults (infections) and diseases in other organ systems.
One recent project that’s attracted Malcolm’s attention is understanding how immune cells repair the kidney after acute kidney injury. “The incidence of acute kidney injury is increasing globally,” says Malcolm. “We know that there is a strong association between acute kidney injury and the development of chronic kidney disease, so that’s where I’m focussed.”
Exploring the factors that regulate innate lymphoid cells (ILCs) and their role in tissue maintenance and repair, Malcolm is leads a team looking to explore chronic kidney diseases. Around 1.7 million Australians have kidney disease, a condition which contributes to approximately 14 per cent of all Australian deaths.
Working with a team of local and global researchers, Malcolm hopes that this research can play an important role in the understanding of this complex health issue.
Raising hope and raising awareness
Recognised as a leading young researcher in the field of paediatric respiratory medicine after winning the internationally competitive Klosterfrau Grant for research of airway diseases in childhood in 2015, Malcolm points to "tailor-made, personalised medicine" as the science of the not-so-distant future, hoping to pinpoint more discrete subsets of patients and how he can better treat them.
"A critical goal of our research is to understand what factors drive the development of chronic diseases and devise strategies to stop this from occurring."
An insight into the immune system
Dr Malcolm Starkey is a National Health and Medical Research Council (NHMRC) Early Career Postdoctoral Fellow who is using transgenic animal technology to inv
Career Summary
Biography
Dr Starkey is an Australian Research Council (ARC) Discovery Early Career Research Award (DECRA) fellow in the School of Biomedical Science and Pharmacy, Faculty of Health and Medicine. He is based at the Hunter Medical Research Institute as part of the Priority Research Centre's for GrowUpWell and Healthy Lungs.
Dr Starkey is an immunologist and physiologist interested in how respiratory challenges in early-life impair the normal development of the lung and a healthy immune system and how this may predispose to chronic diseases such as asthma, emphysema. He also studies the immune system in the urinary system with a particular focus on kidney injury and stone formation. His work is substantially contributing to understanding the basic molecular and cellular mechanisms driving chronic diseases. Indeed his work has made important contributions and led to the identification of novel therapeutic strategies that are under further investigation. Dr Starkey uses novel mouse models that recapitulate the hallmark features of human disease, including infections of multiple organs, asthma and kidney injury and kidney stones. He employs these models to understand how the immune system works, and to advance knowledge on the fundamental processes underpinning thw disruption of normal physiological function in multiple organs and systems. His work has substantially furthered the understanding of the deleterious effects of infection in early life and how these infections have long-term consequences for the respiratory and immune systems. More recently he has modeled infection-induced severe asthma and emphysema and is identifying strategies for treating these severe forms of disease. This has been achieved using mouse models of human disease and specifically he has shown that:
*1. Chlamydia respiratory tract infection (RTI) in early life differentially suppress (neonates) or enhance (infants) allergic inflammation depending on the age infection. Nevertheless infection at either age increases asthma severity. Published in 2xJ Allergy Clin Immunol IF=12, ERA=A*
*2. Constitutive IL-13 promotes Chlamydia RTI in early life and associated asthma. Published in Mucosal Immunol IF=7.5, ERA=A*
*3. TRAIL and its receptors are required for neonatal Chlamydia RTI-induced asthma. Published in Mucosal Immunol IF=7.5, ERA=A*
4. Infection with Streptococcus pneumoniae suppresses allergic airway disease through the induction of regulatory T cells. Published in Eur Respir J IF=7, ERA=A*
5. Chlamydia RTI during asthma in later life drives more severe asthma with similar features to severe asthma in humans that is dominated by Th1/Th17 responses and airway neutrophilia. Published in J Immunol IF=6, ERA=A*
6. TLR2 but not TLR4 is required for effective host defence against neonatal Chlamydia RTI. Published in PLoS One IF=4, ERA=A
*7. Chlamydia RTI in infants but not neonates alters hematopoietic cells to promote asthma. Published in PLoS One IF=4, ERA=A
8. Targeting PI3K-p110α suppresses influenza viral infection in chronic obstructive pulmonary disease. Accepted Am J Respir Crit Care Med IF =12, ERA=A*
9. Antibiotics (macrolides) suppress key features of experimental steroid-sensitive and steroid-insensitive asthma. Published in Thorax IF= 8.5, ERA=A*
10. PD-L1 promotes early-life infection-induced severe asthma. Published in Am J Respir Cell Mol Biol IF=4, ERA=A
11. He has also written (three) and contributed to multiple reviews and editorials in this field (*Curr Opin Pharmacol (IF=7, ERA=A), Expert Opin Invest Drugs (IF=5, ERA=A), J Devl Orig Health Dis (IF=2, ERA=C), *Clin Obst Gyn (IF=2, ERA=C), *Ann Am Thorac Soc, Thorax). Those marked * are as first author. He has an average impact factor of >7 and >85% of his manuscripts are in ERA ranked A*/A journals. His work has been cited >500 times since 2012.
His achievements during his studies and early post-doctoral career have been recognised by over 20 awards/fellowships, including the prestigious NHMRC Early Career Post-doctoral Fellowship (Doherty), ARC DECRA fellowship, HMRI Early Career Research education prize, University Alumni awards, multiple communication awards, the Faculty of Health Honours Research Medal, international laboratory exchange awards, The Peter Phelan Paediatric fellowship, The Janet Elder International Travel award and numerous scholarships. Dr Starkey was recently awarded the internationally competitive Klosterfrau research grant honouring an outstanding young scientist in the field of paediatric pulmonology. He has presented his work at numerous international and national conferences and institutions including Harvard, Imperial College, University of London and Cardiff University.
Research Expertise
Our research involves the use of well-established models of respiratory bacterial and viral infections to understand the immunological mechanisms underpinning the development of chronic respiratory diseases such as asthma and emphysema. A particular interest is how infections in early-life predispose to disease in later-life. We are also exploring how respiratory infections exacerbate existing lung disease such as asthma and chronic obstructive pulmonary disease (COPD). We have models of Chlamydia, Streptococcus pneumoniae, Haemophilus influenzae, Influenza, Respiratory syncytial virus, Rhinovirus, and Pseudomonas aeruginosa respiratory infections that we superimpose with models of asthma and emphysema/COPD. We investigate the role of specific molecules in these systems using transgenic animal models (knock-out, knock-in, reporter systems) and inhibitory compounds (monoclonal antibodies, small molecule inhibitors) to identify potential therapeutic targets. We also adopt a translational approach where we take our key observations from our models and look for these molecules/pathways in human tissue.
In more recent studies, we have become interested in the basic process underpinning normal mammalian lung development. We hypothesise that the immune system plays a currently unknown role in regulating stem cell maintenance and lung development. We are also investigating the role of innate lymphoid cells in kidney injury and repair.
Teaching Expertise
Lecturer, laboratory demonstrator and tutor of all levels of the B Biomedical Science program at the University of Newcastle. The supervisor of several summer scholarship, HUBS3409 (3rd year projects), honours and PhD students.
Administrative Expertise
Collaborations
University of Newcastle/Hunter Medical Research Institute collaborators; - Prof. Phil Hansbro - Dr Jay Horvat - Prof. Paul Foster - Prof. Peter Wark - Dr Alan Hsu - Prof. Darryl Knight - Dr Fatemeh Moheimani - Prof. Joerg Mattes - Dr Adam Collison - Dr Matt Dun - Dr Jamie Flynn, Prof. Lisa Wood. External Australian collaborators; - Prof. Ranjeny Thomas University of Queensland - Dr. Brendan O'Sullivan University of Queensland - A/Prof. Ray Steptoe University of Queensland - Dr Stavros Selemidis Monash University - Dr Sandra Nicholson Walter and Eliza Hall Institute of Medical Research, Prof. Gabrielle Belz Walter and Eliza Hall Institute of Medical Research, International collaborators; - Prof. Hideo Yagita Juntendo University Japan - Prof. Ian Adcock Imperial College London - Prof. Mark Inman McMaster University Canada - Dr Jeremy Hirota The University of British Columbia - Prof. Andrew McKenzie University of Cambridge
Qualifications
- PhD (Immunology and Microbiology), University of Newcastle
- Bachelor of Biomedical Sciences, University of Newcastle
- Bachelor of Biomedical Sciences (Hons), University of Newcastle
Keywords
- Acute Kidney Injury
- Asthma
- Chlamydia
- Chronic Obstructive Pulmonary Disease (COPD)
- Early life infections
- Emphysema
- IL-22
- IL-33
- ILC2
- Immunology
- Influenza
- Innate lymphoid cells
- Kidney
- Lung development
- Lung diseases
- Neonate
- Respiratory infections
Languages
- English (Mother)
Fields of Research
Code | Description | Percentage |
---|---|---|
320499 | Immunology not elsewhere classified | 50 |
310799 | Microbiology not elsewhere classified | 25 |
320214 | Nephrology and urology | 25 |
Professional Experience
Academic appointment
Dates | Title | Organisation / Department |
---|---|---|
1/7/2020 - | Lab Head | Monash University Department of Immunology and Pathology Australia |
1/7/2017 - 30/6/2020 |
ARC DECRA Fellow Australian Research Council (ARC) Discovery Early Career Researcher Award (DECRA) |
ARC (Australian Research Council) Australia |
1/1/2017 - 30/6/2020 |
Lecturer Research only Level B academic/research fellow |
The University of Newcastle Immunology and Microbiology, School of Biomedical Sciences and Pharmacy Australia |
1/1/2014 - | NHMRC Early Career Post-doctoral Fellow | University of Newcastle School of Biomedical Sciences and Pharmacy Australia |
1/1/2014 - |
NHMRC early career fellow NHMRC - Early Career Fellowships (Formerly Postdoctoral Training Fellowships) |
University of Newcastle Australia |
1/1/2014 - | Membership - International Cytokine and Interferon Society | International Cytokine and Interferon Society Australia |
1/10/2013 - 1/1/2014 | Associate Lecturer | University of Newcastle Australia |
1/1/2010 - 31/12/2015 | Membership - Australian Lung Foundation | Lung Foundation Australia |
1/1/2010 - 31/12/2015 | Membership - Thoracic Society of Australia and New Zealand | The Thoracic Society of Australia and New Zealand Australia |
1/1/2010 - 31/12/2013 | Conference Chair - Newcastle Asthma Meeting | Newcastle Asthma Meeting Australia |
1/1/2008 - 31/12/2015 | Membership - Australasian Society of Immunology | Australasian Society of Immunology Australia |
Awards
Award
Year | Award |
---|---|
2016 |
Science at The Shine Dome Early Career Travel Award Australian Academy of Sciences |
2016 |
Monash Department of Immunology and Pathology Travel Bursay Monash University |
2015 |
Australasian Society Immunology Travel Award Australasian Society of Immunology |
Distinction
Year | Award |
---|---|
2008 |
Faculty of Health and Medicine Medal University of Newcastle |
Nomination
Year | Award |
---|---|
2016 |
Finalist Young Alumni Awards The University of Newcastle |
Recognition
Year | Award |
---|---|
2015 |
Thoracic Society of Australia and New Zealand (TSANZ) conference travel award Unknown |
2014 |
Priority Research Centre for Asthma and Respiratory Disease early career award Unknown |
2014 |
University of Newcastle, research conference travel grant University of Newcastle |
2013 |
Priority Research Centre for Asthma and Respiratory Disease student award Unknown |
2012 |
Australasian Society of Immunology travel grant Australasian Society of Immunology |
2012 |
New Investigator Award at Australasian Society of Immunology annual meeting Unknown |
2011 |
Science communication award at the Australasian Society of Immunology annual meeting Australasian Society of Immunology |
Research Award
Year | Award |
---|---|
2016 |
ARC Discovery Early Career Researcher Award (DECRA) ARC (Australian Research Council) |
2015 |
Klosterfrau research grant Unknown |
2015 |
Janet Elder International travel award Thoracic Society of Australia and New Zealand |
2014 |
The Leo Dintenfass Memorial Award for research excellence Unknown |
2014 |
Peter Phelan Pediatric Travel Grant Unknown |
2014 |
International Cytokine and Interferon Society travel award Unknown |
2012 |
International laboratory exchange award Unknown |
2011 |
PULSE Education Prize Unknown |
2009 |
Cooperative Research Council for Asthma and Airways international travel award Unknown |
2008 |
Australian postgraduate award Unknown |
2008 |
Asthma Foundation PhD Scholarship Unknown |
Invitations
Speaker
Year | Title / Rationale |
---|---|
2015 |
Early-life infections and chronic lung disease Organisation: Imperial College London |
2015 |
Early-life infections and the development of asthma Organisation: Brigham and Women's Hospital and Harvard Medical School |
Publications
For publications that are currently unpublished or in-press, details are shown in italics.
Journal article (74 outputs)
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2024 |
Mayall JR, Horvat JC, Mangan NE, Chevalier A, McCarthy H, Hampsey D, et al., 'Interferon-epsilon is a novel regulator of NK cell responses in the uterus', EMBO Molecular Medicine, 16 267-293 [C1]
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2023 |
Eliezer DD, Lam C, Smith A, Coomarasamy JM, Samnakay N, Starkey MR, Deshpande AV, 'Optimising the management of children with concomitant bladder dysfunction and behavioural disorders', EUROPEAN CHILD & ADOLESCENT PSYCHIATRY, 32 1989-1999 (2023) [C1]
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2023 |
Nguyen TTH, Starkey MR, 'Shining the spotlight on urinary tract immunology', Mucosal Immunology, 16 563-566 (2023)
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2023 |
Cao Q, Wang R, Niu Z, Chen T, Azmi F, Read SA, et al., 'Type 2 innate lymphoid cells are protective against hepatic ischaemia/reperfusion injury', JHEP Reports, 5 (2023) [C1] Background and Aims: Although type 2 innate lymphoid cells (ILC2s) were originally found to be liver-resident lymphocytes, the role and importance of ILC2 in liver injury remains ... [more] Background and Aims: Although type 2 innate lymphoid cells (ILC2s) were originally found to be liver-resident lymphocytes, the role and importance of ILC2 in liver injury remains poorly understood. In the current study, we sought to determine whether ILC2 is an important regulator of hepatic ischaemia/reperfusion injury (IRI). Methods: ILC2-deficient mice (ICOS-T or NSG) and genetically modified ILC2s were used to investigate the role of ILC2s in murine hepatic IRI. Interactions between ILC2s and eosinophils or macrophages were studied in coculture. The role of human ILC2s was assessed in an immunocompromised mouse model of hepatic IRI. Results: Administration of IL-33 prevented hepatic IRI in association with reduction of neutrophil infiltration and inflammatory mediators in the liver. IL-33-treated mice had elevated numbers of ILC2s, eosinophils, and regulatory T cells. Eosinophils, but not regulatory T cells, were required for IL-33-mediated hepatoprotection in IRI mice. Depletion of ILC2s substantially abolished the protective effect of IL-33 in hepatic IRI, indicating that ILC2s play critical roles in IL-33-mediated liver protection. Adoptive transfer of ex vivo-expanded ILC2s improved liver function and attenuated histologic damage in mice subjected to IRI. Mechanistic studies combining genetic and adoptive transfer approaches identified a protective role of ILC2s through promoting IL-13-dependent induction of anti-inflammatory macrophages and IL-5-dependent elevation of eosinophils in IRI. Furthermore, in vivo expansion of human ILC2s by IL-33 or transfer of ex vivo-expanded human ILC2s ameliorated hepatic IRI in an immunocompromised mouse model of hepatic IRI. Conclusions: This study provides insight into the mechanisms of ILC2-mediated liver protection that could serve as therapeutic targets to treat acute liver injury. Impact and Implications: We report that type 2 innate lymphoid cells (ILC2s) are important regulators in a mouse model of liver ischaemia/reperfusion injury (IRI). Through manipulation of macrophage and eosinophil phenotypes, ILC2s mitigate liver inflammation and injury during liver IRI. We propose that ILC2s have the potential to serve as a therapeutic tool for protecting against acute liver injury and lay the foundation for translation of ILC2 therapy to human liver disease.
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2023 |
Girkin JLN, Sokulsky LA, Starkey MR, Hansbro PM, Foster PS, Collison AM, Mattes J, 'A unique role for IL-13 in inducing esophageal eosinophilia through MID-1 and STAT6', Frontiers in Allergy, 4 [C1]
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2023 |
Bhatt NP, Deshpande AV, Starkey MR, 'Pharmacological interventions for the management of cystinuria: a systematic review.', J Nephrol, (2023) [C1]
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2023 |
Liu G, Haw TJ, Starkey MR, Philp AM, Pavlidis S, Nalkurthi C, et al., 'TLR7 promotes smoke-induced experimental lung damage through the activity of mast cell tryptase.', Nat Commun, 14 7349 (2023) [C1]
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2023 |
Hardy SA, Liesinger L, Patrick R, Poettler M, Rech L, Gindlhuber J, et al., 'Extracellular Matrix Protein-1 as a Mediator of Inflammation-Induced Fibrosis After Myocardial Infarction', JACC: Basic to Translational Science, 8 1539-1554 (2023) [C1]
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2022 |
Pinkerton JW, Kim RY, Brown AC, Rae BE, Donovan C, Mayall JR, et al., 'Relationship between type 2 cytokine and inflammasome responses in obesity-associated asthma', JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 149 1270-1280 (2022) [C1]
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Nova | |||||||||
2022 |
Vavilov S, Roberts E, Smith GHH, Starkey M, Pockney P, Deshpande AV, 'Parental decision regret among Australian parents after consenting to or refusing hypospadias repair for their son: Results of a survey with controls.', J Pediatr Urol, 18 482-488 (2022) [C1]
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2022 |
Lao JC, Bui CB, Pang MA, Cho SX, Rudloff I, Elgass K, et al., 'Type 2 immune polarization is associated with cardiopulmonary disease in preterm infants', Science Translational Medicine, 14 (2022) [C1] Postnatal maturation of the immune system is poorly understood, as is its impact on illnesses afflicting term or preterm infants, such as bronchopulmonary dysplasia (BPD) and BPD-... [more] Postnatal maturation of the immune system is poorly understood, as is its impact on illnesses afflicting term or preterm infants, such as bronchopulmonary dysplasia (BPD) and BPD-associated pulmonary hypertension. These are both cardiopulmonary inflammatory diseases that cause substantial mortality and morbidity with high treatment costs. Here, we characterized blood samples collected from 51 preterm infants longitudinally at five time points, 20 healthy term infants at birth and age 3 to 16 weeks, and 5 healthy adults. We observed strong associations between type 2 immune polarization in circulating CD3+CD4+ T cells and cardiopulmonary illness, with odds ratios up to 24. Maternal magnesium sulfate therapy, delayed hepatitis B vaccination, and increasing fetal, but not maternal, chorioamnionitis severity were associated with attenuated type 2 polarization. Blocking type 2 mediators such as interleukin-4 (IL-4), IL-5, IL-13, or signal transducer and activator of transcription 6 (STAT6) in murine neonatal cardiopulmonary disease in vivo prevented changes in cell type composition, increases in IL-1ß and IL-13, and losses of pulmonary capillaries, but not gains in larger vessels. Thereby, type 2 blockade ameliorated lung inflammation, protected alveolar and vascular integrity, and confirmed the pathological impact of type 2 cytokines and STAT6. In-depth flow cytometry and single-cell transcriptomics of mouse lungs further revealed complex associations between immune polarization and cardiopulmonary disease. Thus, this work advances knowledge on developmental immunology and its impact on early life disease and identifies multiple therapeutic approaches that may relieve inflammation-driven suffering in the youngest patients.
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2022 |
Hosseini B, Berthon BS, Jensen ME, McLoughlin RF, Wark PAB, Nichol K, et al., 'The Effects of Increasing Fruit and Vegetable Intake in Children with Asthma on the Modulation of Innate Immune Responses', Nutrients, 14 3087-3087 (2022) [C1]
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2022 |
Tu X, Kim RY, Brown AC, de Jong E, Jones-Freeman B, Ali MK, et al., 'Airway and parenchymal transcriptomics in a novel model of asthma and COPD overlap', Journal of Allergy and Clinical Immunology, 150 817-829.e6 (2022) [C1] Background: Asthma and chronic obstructive pulmonary disease (COPD) are common chronic respiratory diseases, and some patients have overlapping disease features, termed asthma-COP... [more] Background: Asthma and chronic obstructive pulmonary disease (COPD) are common chronic respiratory diseases, and some patients have overlapping disease features, termed asthma-COPD overlap (ACO). Patients characterized with ACO have increased disease severity; however, the mechanisms driving this have not been widely studied. Objectives: This study sought to characterize the phenotypic and transcriptomic features of experimental ACO in mice induced by chronic house dust mite antigen and cigarette smoke exposure. Methods: Female BALB/c mice were chronically exposed to house dust mite antigen for 11 weeks to induce experimental asthma, cigarette smoke for 8 weeks to induce experimental COPD, or both concurrently to induce experimental ACO. Lung inflammation, structural changes, and lung function were assessed. RNA-sequencing was performed on separated airway and parenchyma lung tissues to assess transcriptional changes. Validation of a novel upstream driver SPI1 in experimental ACO was assessed using the pharmacological SPI1 inhibitor, DB2313. Results: Experimental ACO recapitulated features of both asthma and COPD, with mixed pulmonary eosinophilic/neutrophilic inflammation, small airway collagen deposition, and increased airway hyperresponsiveness. Transcriptomic analysis identified common and distinct dysregulated gene clusters in airway and parenchyma samples in experimental asthma, COPD, and ACO. Upstream driver analysis revealed increased expression of the transcription factor Spi1. Pharmacological inhibition of SPI1 using DB2313, reduced airway remodeling and airway hyperresponsiveness in experimental ACO. Conclusions: A new experimental model of ACO featuring chronic dual exposures to house dust mite and cigarette smoke mimics key disease features observed in patients with ACO and revealed novel disease mechanisms, including upregulation of SPI1, that are amenable to therapy.
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2021 |
Kuchibhotla VNS, Starkey MR, Reid AT, Heijink IH, Nawijn MC, Hansbro PM, Knight DA, 'Inhibition of beta-Catenin/CREB Binding Protein Signaling Attenuates House Dust Mite-Induced Goblet Cell Metaplasia in Mice', FRONTIERS IN PHYSIOLOGY, 12 (2021) [C1]
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2021 |
Berthon BS, McLoughlin RF, Jensen ME, Hosseini B, Williams EJ, Baines KJ, et al., 'The effects of increasing fruit and vegetable intake in children with asthma: A randomized controlled trial', CLINICAL AND EXPERIMENTAL ALLERGY, 51 1144-1156 (2021) [C1]
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2021 |
Hosseini B, Berthon BS, Starkey MR, Collison A, McLoughlin RF, Williams EJ, et al., 'Children With Asthma Have Impaired Innate Immunity and Increased Numbers of Type 2 Innate Lymphoid Cells Compared With Healthy Controls', FRONTIERS IN IMMUNOLOGY, 12 (2021) [C1]
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2021 |
Martins Costa Gomes G, de Gouveia Belinelo P, Starkey MR, Murphy VE, Hansbro PM, Sly PD, et al., 'Cord blood group 2 innate lymphoid cells are associated with lung function at 6 weeks of age', CLINICAL & TRANSLATIONAL IMMUNOLOGY, 10 (2021) [C1]
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2021 |
Gomes GMC, Karmaus W, Murphy VE, Gibson PG, Percival E, Hansbro PM, et al., 'Environmental Air Pollutants Inhaled during Pregnancy Are Associated with Altered Cord Blood Immune Cell Profiles', INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH, 18 (2021) [C1]
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2021 |
Loering S, Cameron GJM, Bhatt NP, Belz GT, Foster PS, Hansbro PM, Starkey MR, 'Differences in pulmonary group 2 innate lymphoid cells are dependent on mouse age, sex and strain', IMMUNOLOGY AND CELL BIOLOGY, 99 542-551 (2021) [C1]
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2021 |
Eliezer DD, Samnakay N, Starkey MR, Deshpande AV, 'Effectiveness of standard urotherapy (basic bladder advice) and combination therapies in managing bladder dysfunction in children with treated behavioral disorders: Results of a prospective cohort (DABBED) study', LUTS-LOWER URINARY TRACT SYMPTOMS, 13 490-497 (2021) [C1]
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2021 |
Lea-Henry TN, Chuah A, Stanley M, Athanasopoulos V, Starkey MR, Christiadi D, et al., 'Increased burden of rare variants in genes of the endosomal Toll-like receptor pathway in patients with systemic lupus erythematosus', Lupus, 30 1756-1763 (2021) [C1] Objective: To compare the frequency of rare variants in genes of the pathophysiologically relevant endosomal Toll-like receptor (eTLR) pathway and any quantifiable differences in ... [more] Objective: To compare the frequency of rare variants in genes of the pathophysiologically relevant endosomal Toll-like receptor (eTLR) pathway and any quantifiable differences in variant rarity, predicted deleteriousness, or molecular proximity in patients with systemic lupus erythematosus (SLE) and healthy controls. Patients and methods: 65 genes associated with the eTLR pathway were identified by literature search and pathway analysis. Using next generation sequencing techniques, these were compared in two randomised cohorts of patients with SLE (n = 114 and n = 113) with 197 healthy controls. Genetically determined ethnicity was used to normalise minor allele frequencies (MAF) for the identified genetic variants and these were then compared by their frequency: rare (MAF < 0.005), uncommon (MAF 0.005¿0.02), and common (MAF >0.02). This was compared to the results for 65 randomly selected genes. Results: Patients with SLE are more likely to carry a rare nonsynonymous variant affecting proteins within the eTLR pathway than healthy controls. Furthermore, individuals with SLE are more likely to have multiple rare variants in this pathway. There were no differences in rarity, Combined Annotation Dependent Depletion (CADD) score, or molecular proximity for rare eTLR pathway variants. Conclusions: Rare non-synonymous variants are enriched in patients with SLE in the eTLR pathway. This supports the hypothesis that SLE arises from several rare variants of relatively large effect rather than many common variants of small effect.
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2021 |
Jones-Freeman B, Chonwerawong M, Marcelino VR, Deshpande AV, Forster SC, Starkey MR, 'The microbiome and host mucosal interactions in urinary tract diseases', Mucosal Immunology, 14 779-792 (2021) [C1] The urinary tract consists of the bladder, ureters, and kidneys, and is an essential organ system for filtration and excretion of waste products and maintaining systemic homeostas... [more] The urinary tract consists of the bladder, ureters, and kidneys, and is an essential organ system for filtration and excretion of waste products and maintaining systemic homeostasis. In this capacity, the urinary tract is impacted by its interactions with other mucosal sites, including the genitourinary and gastrointestinal systems. Each of these sites harbors diverse ecosystems of microbes termed the microbiota, that regulates complex interactions with the local and systemic immune system. It remains unclear whether changes in the microbiota and associated metabolites may be a consequence or a driver of urinary tract diseases. Here, we review the current literature, investigating the impact of the microbiota on the urinary tract in homeostasis and disease including urinary stones, acute kidney injury, chronic kidney disease, and urinary tract infection. We propose new avenues for exploration of the urinary microbiome using emerging technology and discuss the potential of microbiome-based medicine for urinary tract conditions.
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2020 |
Vavilov S, Smith G, Starkey M, Pockney P, Deshpande AV, 'Parental decision regret in childhood hypospadias surgery: A systematic review', Journal of Paediatrics and Child Health, 56 1514-1520 (2020) [C1] We conducted a systematic review of the literature to establish the prevalence of and predictive factors for parental decision regret in hypospadias surgery. A search strategy wit... [more] We conducted a systematic review of the literature to establish the prevalence of and predictive factors for parental decision regret in hypospadias surgery. A search strategy without language restrictions was developed with expert help, and two reviewers undertook independent study selection. Five studies were included in this review (four for quantitative analysis) with a total of 783 participants. The mean overall prevalence of parental decision regret was 65.2% (moderate to severe ¿ 20.3%). Although significant predictors of regret were identified (post-operative complications, small size glans, meatal location, decision conflict between parents, parental educational level and others), they had unexplained discordance between studies. Parental decision regret after proximal hypospadias surgery and refusing surgery was inadequately reported. In conclusion, even though the prevalence of parental decision regret after consenting for the hypospadias repair appears to be high, risk factors associated with it were discordant suggesting imprecision in estimates due to unknown confounders.
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2020 |
Ali MK, Kim RY, Brown AC, Mayall JR, Karim R, Pinkerton JW, et al., 'Crucial role for lung iron level and regulation in the pathogenesis and severity of asthma', EUROPEAN RESPIRATORY JOURNAL, 55 (2020) [C1]
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2020 |
Ingersoll MA, Starkey MR, 'Interleukin-22 in urinary tract disease - new experimental directions', CLINICAL & TRANSLATIONAL IMMUNOLOGY, 9 (2020) [C1]
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2019 |
Donovan C, Starkey MR, Kim RY, Rana BMJ, Barlow JL, Jones B, et al., 'Roles for T/B lymphocytes and ILC2s in experimental chronic obstructive pulmonary disease', Journal of Leukocyte Biology, 105 143-150 (2019) [C1] Pulmonary inflammation in chronic obstructive pulmonary disease (COPD) is characterized by both innate and adaptive immune responses; however, their specific roles in the pathogen... [more] Pulmonary inflammation in chronic obstructive pulmonary disease (COPD) is characterized by both innate and adaptive immune responses; however, their specific roles in the pathogenesis of COPD are unclear. Therefore, we investigated the roles of T and B lymphocytes and group 2 innate lymphoid cells (ILC2s) in airway inflammation and remodelling, and lung function in an experimental model of COPD using mice that specifically lack these cells (Rag1 -/- and Rora fl/fl Il7r Cre [ILC2-deficient] mice). Wild-type (WT) C57BL/6 mice, Rag1 -/- , and Rora fl/fl Il7r Cre mice were exposed to cigarette smoke (CS; 12 cigarettes twice a day, 5 days a week) for up to 12¿weeks, and airway inflammation, airway remodelling (collagen deposition and alveolar enlargement), and lung function were assessed. WT, Rag1 -/- , and ILC2-deficient mice exposed to CS had similar levels of airway inflammation and impaired lung function. CS exposure increased small airway collagen deposition in WT mice. Rag1 -/- normal air- and CS-exposed mice had significantly increased collagen deposition compared to similarly exposed WT mice, which was associated with increases in IL-33, IL-13, and ILC2 numbers. CS-exposed Rora fl/fl Il7r Cre mice were protected from emphysema, but had increased IL-33/IL-13 expression and collagen deposition compared to WT CS-exposed mice. T/B lymphocytes and ILC2s play roles in airway collagen deposition/fibrosis, but not inflammation, in experimental COPD.
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2019 |
Hardy SA, Mabotuwana NS, Murtha LA, Coulter B, Sanchez-Bezanilla S, Al-Omary MS, et al., 'Novel role of extracellular matrix protein 1 (ECM1) in cardiac aging and myocardial infarction', PLoS ONE, 14 (2019) [C1] Introduction The prevalence of heart failure increases in the aging population and following myocardial infarction (MI), yet the extracellular matrix (ECM) remodeling underpinning... [more] Introduction The prevalence of heart failure increases in the aging population and following myocardial infarction (MI), yet the extracellular matrix (ECM) remodeling underpinning the development of aging- and MI-associated cardiac fibrosis remains poorly understood. A link between inflammation and fibrosis in the heart has long been appreciated, but has mechanistically remained undefined. We investigated the expression of a novel protein, extracellular matrix protein 1 (ECM1) in the aging and infarcted heart. Methods Young adult (3-month old) and aging (18-month old) C57BL/6 mice were assessed. Young mice were subjected to left anterior descending artery-ligation to induce MI, or transverse aortic constriction (TAC) surgery to induce pressure-overload cardiomyopathy. Left ventricle (LV) tissue was collected early and late post-MI/TAC. Bone marrow cells (BMCs) were isolated from young healthy mice, and subject to flow cytometry. Human cardiac fibroblast (CFb), myocyte, and coronary artery endothelial & smooth muscle cell lines were cultured; human CFbs were treated with recombinant ECM1. Primary mouse CFbs were cultured and treated with recombinant angiotensin-II or TGF-ß1. Immunoblotting, qPCR and mRNA fluorescent in-situ hybridization (mRNA-FISH) were conducted on LV tissue and cells. Results ECM1 expression was upregulated in the aging LV, and in the infarct zone of the LV early post-MI. No significant differences in ECM1 expression were found late post-MI or at any time-point post-TAC. ECM1 was not expressed in any resident cardiac cells, but ECM1 was highly expressed in BMCs, with high ECM1 expression in granulocytes. Flow cytometry of bone marrow revealed ECM1 expression in large granular leucocytes. mRNA-FISH revealed that ECM1 was indeed expressed by inflammatory cells in the infarct zone at day-3 post-MI. ECM1 stimulation of CFbs induced ERK1/2 and AKT activation and collagen-I expression, suggesting a pro-fibrotic role. Conclusions ECM1 expression is increased in ageing and infarcted hearts but is not expressed by resident cardiac cells. Instead it is expressed by bone marrow-derived granulocytes. ECM1 is sufficient to induce cardiac fibroblast stimulation in vitro. Our findings suggest ECM1 is released from infiltrating inflammatory cells, which leads to cardiac fibroblast stimulation and fibrosis in aging and MI. ECM1 may be a novel intermediary between inflammation and fibrosis.
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2019 |
Collison AM, Li J, de Siqueira AP, Lv X, Toop HD, Morris JC, et al., 'TRAIL signals through the ubiquitin ligase MID1 to promote pulmonary fibrosis', BMC PULMONARY MEDICINE, 19 (2019) [C1]
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2019 |
Nair PM, Starkey MR, Haw TJ, Liu G, Collison AM, Mattes J, et al., 'Enhancing tristetraprolin activity reduces the severity of cigarette smoke-induced experimental chronic obstructive pulmonary disease', CLINICAL & TRANSLATIONAL IMMUNOLOGY, 8 (2019) [C1]
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2019 |
Cameron GJM, Jiang SH, Loering S, Deshpande AV, Hansbro PM, Starkey MR, 'Emerging therapeutic potential of group 2 innate lymphoid cells in acute kidney injury', Journal of Pathology, 248 9-15 (2019) [C1] Acute kidney injury (AKI) remains a global challenge and, despite the availability of dialysis and transplantation, can be fatal. Those that survive an AKI are at increased risk o... [more] Acute kidney injury (AKI) remains a global challenge and, despite the availability of dialysis and transplantation, can be fatal. Those that survive an AKI are at increased risk of developing chronic kidney disease and end stage renal failure. Understanding the fundamental mechanisms underpinning the pathophysiology of AKI is critical for developing novel strategies for diagnosis and treatment. A growing body of evidence indicates that amplifying type 2 immunity may have therapeutic potential in kidney injury and disease. Of particular interest are the recently described subset of innate immune cells, termed group 2 innate lymphoid cells (ILCs). Group 2 ILCs are crucial tissue-resident immune cells that maintain homeostasis and regulate tissue repair at multiple organ sites, including the kidney. They are critical mediators of type 2 immune responses following infection and injury. The existing literature suggests that activation of group 2 ILCs and production of a local type 2 immune milieu is protective against renal injury and associated pathology. In this review, we describe the emerging role for group 2 ILCs in renal homeostasis and repair. We provide an in-depth discussion of the most recent literature that use preclinical models of AKI and assess the therapeutic effect of modulating group 2 ILC function. We debate the potential for targeting these cells as novel cellular therapies in AKI and discuss the implications for future studies and translation. Copyright © 2019 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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2019 |
Starkey MR, Plank MW, Casolari P, Papi A, Pavlidis S, Guo Y, et al., 'IL-22 and its receptors are increased in human and experimental COPD and contribute to pathogenesis', EUROPEAN RESPIRATORY JOURNAL, 54 (2019) [C1]
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2019 |
Cameron GJM, Cautivo KM, Loering S, Jiang SH, Deshpande AV, Foster PS, et al., 'Group 2 Innate Lymphoid Cells Are Redundant in Experimental Renal Ischemia-Reperfusion Injury', Frontiers in Immunology, 10 (2019) [C1]
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2019 |
Starkey MR, McKenzie AN, Belz GT, Hansbro PM, 'Pulmonary group 2 innate lymphoid cells: surprises and challenges', Mucosal Immunology, 12 299-311 (2019) [C1] Group 2 innate lymphoid cells (ILC2s) are a recently described subset of innate lymphocytes with important immune and homeostatic functions at multiple tissue sites, especially th... [more] Group 2 innate lymphoid cells (ILC2s) are a recently described subset of innate lymphocytes with important immune and homeostatic functions at multiple tissue sites, especially the lung. These cells expand locally after birth and during postnatal lung maturation and are present in the lung and other peripheral organs. They are modified by a variety of processes and mediate inflammatory responses to respiratory pathogens, inhaled allergens and noxious particles. Here, we review the emerging roles of ILC2s in pulmonary homeostasis and discuss recent and surprising advances in our understanding of how hormones, age, neurotransmitters, environmental challenges, and infection influence ILC2s. We also review how these responses may underpin the development, progression and severity of pulmonary inflammation and chronic lung diseases and highlight some of the remaining challenges for ILC2 biology.
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2019 |
Loering S, Cameron GJM, Starkey MR, Hansbro PM, 'Lung development and emerging roles for type 2 immunity', Journal of Pathology, 247 686-696 (2019) [C1] Lung development is a complex process mediated through the interaction of multiple cell types, factors and mediators. In mice, it starts as early as embryonic day 9 and continues ... [more] Lung development is a complex process mediated through the interaction of multiple cell types, factors and mediators. In mice, it starts as early as embryonic day 9 and continues into early adulthood. The process can be separated into five different developmental stages: embryonic, pseudoglandular, canalicular, saccular, and alveolar. Whilst lung bud formation and branching morphogenesis have been studied extensively, the mechanisms of alveolarisation are incompletely understood. Aberrant lung development can lead to deleterious consequences for respiratory health such as bronchopulmonary dysplasia (BPD), a disease primarily affecting preterm neonates, which is characterised by increased pulmonary inflammation and disturbed alveolarisation. While the deleterious effects of type 1-mediated inflammatory responses on lung development have been well established, the role of type 2 responses in postnatal lung development remains poorly understood. Recent studies indicate that type 2-associated immune cells, such as group 2 innate lymphoid cells and alveolar macrophages, are increased in number during postnatal alveolarisation. Here, we present the current state of understanding of the postnatal stages of lung development and the key cell types and mediators known to be involved. We also provide an overview of how stem cells are involved in lung development and regeneration, and the negative influences of respiratory infections. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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2018 |
Nair PM, Starkey MR, Haw TJ, Ruscher R, Liu G, Maradana MR, et al., 'RelB-deficient Dendritic Cells Promote the Development of Spontaneous Allergic Airway Inflammation.', American journal of respiratory cell and molecular biology, (2018) [C1]
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2018 |
Periyalil HA, Wood LG, Wright TA, Karihaloo C, Starkey MR, Miu AS, et al., 'Obese asthmatics are characterized by altered adipose tissue macrophage activation', CLINICAL AND EXPERIMENTAL ALLERGY, 48 641-649 (2018) [C1]
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2018 |
Haw TJ, Starkey MR, Pavlidis S, Fricker M, Arthurs AL, Nair PM, et al., 'Toll-like receptor 2 and 4 have opposing roles in the pathogenesis of cigarette smoke-induced chronic obstructive pulmonary disease.', American journal of physiology. Lung cellular and molecular physiology, 314 L298-L317 (2018) [C1]
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2018 |
Hosseini B, Berthon BS, Saedisomeolia A, Starkey MR, Collison A, Wark PAB, Wood LG, 'Effects of fruit and vegetable consumption on inflammatory biomarkers and immune cell populations: a systematic literature review and meta-analysis.', The American journal of clinical nutrition, 108 136-155 (2018) [C1]
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2017 |
Hansbro PM, Kim RY, Starkey MR, Donovan C, Dua K, Mayall JR, et al., 'Mechanisms and treatments for severe, steroid-resistant allergic airway disease and asthma', Immunological Reviews, 278 41-62 (2017) [C1] Severe, steroid-resistant asthma is clinically and economically important since affected individuals do not respond to mainstay corticosteroid treatments for asthma. Patients with... [more] Severe, steroid-resistant asthma is clinically and economically important since affected individuals do not respond to mainstay corticosteroid treatments for asthma. Patients with this disease experience more frequent exacerbations of asthma, are more likely to be hospitalized, and have a poorer quality of life. Effective therapies are urgently required, however, their development has been hampered by a lack of understanding of the pathological processes that underpin disease. A major obstacle to understanding the processes that drive severe, steroid-resistant asthma is that the several endotypes of the disease have been described that are characterized by different inflammatory and immunological phenotypes. This heterogeneity makes pinpointing processes that drive disease difficult in humans. Clinical studies strongly associate specific respiratory infections with severe, steroid-resistant asthma. In this review, we discuss key findings from our studies where we describe the development of representative experimental models to improve our understanding of the links between infection and severe, steroid-resistant forms of this disease. We also discuss their use in elucidating the mechanisms, and their potential for developing effective therapeutic strategies, for severe, steroid-resistant asthma. Finally, we highlight how the immune mechanisms and therapeutic targets we have identified may be applicable to obesity-or pollution-associated asthma.
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2017 |
Hansbro PM, Haw TJ, Starkey MR, Miyake K, 'Toll-like receptors in COPD', EUROPEAN RESPIRATORY JOURNAL, 49 (2017) [C1]
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2017 |
Nair PM, Starkey MR, Haw TJ, Liu G, Horvat JC, Morris JC, et al., 'Targeting PP2A and proteasome activity ameliorates features of allergic airway disease in mice', Allergy: European Journal of Allergy and Clinical Immunology, 72 1891-1903 (2017) [C1] Background: Asthma is an allergic airway disease (AAD) caused by aberrant immune responses to allergens. Protein phosphatase-2A (PP2A) is an abundant serine/threonine phosphatase ... [more] Background: Asthma is an allergic airway disease (AAD) caused by aberrant immune responses to allergens. Protein phosphatase-2A (PP2A) is an abundant serine/threonine phosphatase with anti-inflammatory activity. The ubiquitin proteasome system (UPS) controls many cellular processes, including the initiation of inflammatory responses by protein degradation. We assessed whether enhancing PP2A activity with fingolimod (FTY720) or 2-amino-4-(4-(heptyloxy) phenyl)-2-methylbutan-1-ol (AAL (S) ), or inhibiting proteasome activity with bortezomib (BORT), could suppress experimental AAD. Methods: Acute AAD was induced in C57BL/6 mice by intraperitoneal sensitization with ovalbumin (OVA) in combination with intranasal (i.n) exposure to OVA. Chronic AAD was induced in mice with prolonged i.n exposure to crude house dust mite (HDM) extract. Mice were treated with vehicle, FTY720, AAL (S) , BORT or AAL (S) +BORT and hallmark features of AAD assessed. Results: AAL (S) reduced the severity of acute AAD by suppressing tissue eosinophils and inflammation, mucus-secreting cell (MSC) numbers, type 2-associated cytokines (interleukin (IL)-33, thymic stromal lymphopoietin, IL-5 and IL-13), serum immunoglobulin (Ig)E and airway hyper-responsiveness (AHR). FTY720 only suppressed tissue inflammation and IgE. BORT reduced bronchoalveolar lavage fluid (BALF) and tissue eosinophils and inflammation, IL-5, IL-13 and AHR. Combined treatment with AAL (S) +BORT had complementary effects and suppressed BALF and tissue eosinophils and inflammation, MSC numbers, reduced the production of type 2 cytokines and AHR. AAL (S) , BORT and AAL (S) +BORT also reduced airway remodelling in chronic AAD. Conclusion: These findings highlight the potential of combination therapies that enhance PP2A and inhibit proteasome activity as novel therapeutic strategies for asthma.
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2017 |
Kim RY, Horvat JC, Pinkerton JW, Starkey MR, Essilfie AT, Mayall JR, et al., 'MicroRNA-21 drives severe, steroid-insensitive experimental asthma by amplifying phosphoinositide 3-kinase mediated suppression of histone deacetylase 2', Journal of Allergy and Clinical Immunology, 139 519-532 (2017) [C1] Background Severe steroid-insensitive asthma is a substantial clinical problem. Effective treatments are urgently required, however, their development is hampered by a lack of und... [more] Background Severe steroid-insensitive asthma is a substantial clinical problem. Effective treatments are urgently required, however, their development is hampered by a lack of understanding of the mechanisms of disease pathogenesis. Steroid-insensitive asthma is associated with respiratory tract infections and noneosinophilic endotypes, including neutrophilic forms of disease. However, steroid-insensitive patients with eosinophil-enriched inflammation have also been described. The¿mechanisms that underpin infection-induced, severe steroid-insensitive asthma can be elucidated by using mouse models of disease. Objective We sought to develop representative mouse models of severe, steroid-insensitive asthma and to use them to identify pathogenic mechanisms and investigate new treatment approaches. Methods Novel mouse models of Chlamydia, Haemophilus influenzae, influenza, and respiratory syncytial virus respiratory¿tract infections and ovalbumin-induced, severe, steroid-insensitive allergic airway disease (SSIAAD) in BALB/c mice were developed and interrogated. Results Infection induced increases in the levels of microRNA (miRNA)-21 (miR-21) expression in the lung during SSIAAD, whereas expression of the miR-21 target phosphatase and tensin homolog was reduced. This was associated with an increase in levels of phosphorylated Akt, an indicator of phosphoinositide 3-kinase (PI3K) activity, and decreased nuclear histone deacetylase (HDAC)2 levels. Treatment with an miR-21¿specific antagomir (Ant-21) increased phosphatase and tensin homolog levels. Treatment with Ant-21, or the pan-PI3K inhibitor LY294002, reduced PI3K activity and restored HDAC2 levels. This led to suppression of airway hyperresponsiveness and restored steroid sensitivity to allergic airway disease. These observations were replicated with SSIAAD associated with 4 different pathogens. Conclusion We identify a previously unrecognized role for an¿miR-21/PI3K/HDAC2 axis in SSIAAD. Our data highlight miR-21 as a novel therapeutic target for the treatment of this form of asthma.
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2017 |
Girkin JL, Hatchwell LM, Collison AM, Starkey MR, Hansbro PM, Yagita H, et al., 'TRAIL signaling is proinflammatory and proviral in a murine model of rhinovirus 1B infection', American Journal of Physiology - Lung Cellular and Molecular Physiology, 312 L89-L99 (2017) [C1] 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 (TRAI... [more] The aim of this study is to elucidate the role of TRAIL during rhinovirus (RV) infection in vivo. Naïve wild-type and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-deficient (Tnfsf10-/-) BALB/c mice were infected intranasally with RV1B. In separate experiments, Tnfsf10-/-mice were sensitized and challenged via the airway route with house dust mite (HDM) to induce allergic airways disease and then challenged with RVIB or UV-RVIB. Airway hyperreactivity (AHR) was invasively assessed as total airways resistance in response to increasing methacholine challenge and inflammation was assessed in bronchoalveolar lavage fluid at multiple time points postinfection. Chemokines were quantified by ELISA of whole lung lysates and viral load was determined by quantitative RT-PCR and tissue culture infective dose (TCID50). Human airway epithelial cells (BEAS2B) were infected with RV1B and stimulated with recombinant TRAIL or neutralizing anti-TRAIL antibodies and viral titer assessed by TCID50. HDM-challenged Tnfsf10-/-mice were protected against RV-induced AHR and had suppressed cellular infiltration in the airways upon RV infection. Chemokine C-X-C-motif ligand 2 (CXCL2) production was suppressed in naïve Tnfsf10-/-mice infected with RV1B, with less RV1B detected 24 h postinfection. This was associated with reduced apoptotic cell death and a reduction of interferon (IFN)-¿2/3 but not IFN-a or IFN-ß. TRAIL stimulation increased, whereas anti-TRAIL antibodies reduced viral replication in RV1B-infected BEAS2B cells in vitro. In conclusion, TRAIL promotes RV-induced AHR, inflammation and RV1B replication, implicating this molecule and its downstream signaling pathways as a possible target for the amelioration of RV1B-induced allergic and nonallergic lung inflammation and AHR.
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2017 |
Ali MK, Kim RY, Karim R, Mayall JR, Martin KL, Shahandeh A, et al., 'Role of iron in the pathogenesis of respiratory disease', INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 88 181-195 (2017) [C1]
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2017 |
Al-Kouba J, Wilkinson AN, Starkey MR, Rudraraju R, Werder RB, Liu X, et al., 'Allergen-encoding bone marrow transfer inactivates allergic T cell responses, alleviating airway inflammation', JCI INSIGHT, 2 (2017) [C1]
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2017 |
Kim RY, Pinkerton JW, Essilfie AT, Robertson AAB, Baines KJ, Brown AC, et al., 'Role for NLRP3 inflammasome-mediated, IL-1ß-dependent responses in severe, steroid-resistant asthma', American Journal of Respiratory and Critical Care Medicine, 196 283-297 (2017) [C1] Rationale: Severe, steroid-resistant asthma is the major unmet need in asthma therapy. Disease heterogeneity and poor understanding of pathogenic mechanisms hampers the identifica... [more] Rationale: Severe, steroid-resistant asthma is the major unmet need in asthma therapy. Disease heterogeneity and poor understanding of pathogenic mechanisms hampers the identification of therapeutic targets. Excessive nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome and concomitant IL-1ß responses occur in chronic obstructive pulmonary disease, respiratory infections, and neutrophilic asthma. However, the direct contributions to pathogenesis, mechanisms involved, and potential for therapeutic targeting remain poorly understood, and are unknown in severe, steroid-resistant asthma. Objectives: To investigate the roles and therapeutic targeting of the NLRP3 inflammasome and IL-1ß in severe, steroid-resistant asthma. Methods: We developed mouse models of Chlamydia and Haemophilus respiratory infection-mediated, ovalbumin-induced severe, steroid-resistant allergic airway disease. These models share the hallmark features of human disease, including elevated airway neutrophils, and NLRP3 inflammasome and IL-1ß responses. The roles and potential for targeting of NLRP3 inflammasome, caspase-1, and IL-1ß responses in experimental severe, steroid-resistant asthma were examined using a highly selective NLRP3 inhibitor, MCC950; the specific caspase-1 inhibitor Ac-YVAD-cho; and neutralizing anti-IL-1ß antibody. Roles for IL-1ß-induced neutrophilic inflammation were examined using IL-1ß and anti-Ly6G. Measurements and Main Results: Chlamydia and Haemophilus infections increase NLRP3, caspase-1, IL-1ß responses that drive steroid-resistant neutrophilic inflammation and airway hyperresponsiveness. Neutrophilic airway inflammation, disease severity, and steroid resistance in human asthma correlate with NLRP3 and IL-1ß expression. Treatment with anti-IL-1ß, Ac- YVAD-cho, and MCC950 suppressed IL-1ß responses and the important steroid-resistant features of disease in mice, whereas IL-1ß administration recapitulated these features. Neutrophil depletion suppressed IL-1ß-induced steroid-resistant airway hyperresponsiveness. Conclusions: NLRP3 inflammasome responses drive experimental severe, steroid-resistant asthma and are potential therapeutic targets in this disease.
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2017 |
Kedzierski L, Tate MD, Hsu AC, Kolesnik TB, Linossi EM, Dagley L, et al., 'Suppressor of cytokine signaling (SOCS)5 ameliorates influenza infection via inhibition of EGFR signaling', eLife, 6 1-27 (2017) [C1]
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2017 |
To EE, Vlahos R, Luong R, Halls ML, Reading PC, King PT, et al., 'Endosomal NOX2 oxidase exacerbates virus pathogenicity and is a target for antiviral therapy', NATURE COMMUNICATIONS, 8 (2017) [C1]
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2017 |
Hsu AC-Y, Dua K, Starkey MR, Haw T-J, Nair PM, Nichol K, et al., 'MicroRNA-125a and -b inhibit A20 and MAVS to promote inflammation and impair antiviral response in COPD', JCI INSIGHT, 2 (2017) [C1]
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2016 |
Kim RY, Rae B, Neal R, Donovan C, Pinkerton J, Balachandran L, et al., 'Elucidating novel disease mechanisms in severe asthma', CLINICAL & TRANSLATIONAL IMMUNOLOGY, 5 (2016) [C1]
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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] Food antigens are common inflammatory triggers in pediatric eosinophilic esophagitis (EoE). TNFrelated apoptosis-inducing ligand (TRAIL) promotes eosinophilic inflammation through... [more] 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.
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2016 |
Russell KE, Chung KF, Clarke CJ, Durham AL, Mallia P, Footitt J, et al., 'The MIF antagonist ISO-1 attenuates corticosteroid-insensitive inflammation and airways hyperresponsiveness in an ozone-induced model of COPD', PLoS ONE, 11 (2016) [C1] Introduction. Macrophage migration inhibitory factor (MIF) is an inflammatory cytokine associated with acute and chronic inflammatory disorders and corticosteroid insensitivity. I... [more] Introduction. Macrophage migration inhibitory factor (MIF) is an inflammatory cytokine associated with acute and chronic inflammatory disorders and corticosteroid insensitivity. Its expression in the airways of patients with chronic obstructive pulmonary disease (COPD), a relatively steroid insensitive inflammatory disease is unclear, however. Methods. Sputum, bronchoalveolar lavage (BAL) macrophages and serum were obtained from nonsmokers, smokers and COPD patients. To mimic oxidative stress-induced COPD, mice were exposed to ozone for six-weeks and treated with ISO-1, a MIF inhibitor, and/or dexamethasone before each exposure. BAL fluid and lung tissue were collected after the final exposure. Airway hyperresponsiveness (AHR) and lung function were measured using whole body plethysmography. HIF-1a binding to the Mif promoter was determined by Chromatin Immunoprecipitation assays. Results. MIF levels in sputum and BAL macrophages from COPD patients were higher than those from non-smokers, with healthy smokers having intermediate levels. MIF expression correlated with that of HIF-1a in all patients groups and in ozone-exposed mice. BAL cell counts, cytokine mRNA and protein expression in lungs and BAL, including MIF, were elevated in ozone-exposed mice and had increased AHR. Dexamethasone had no effect on these parameters in the mouse but ISO-1 attenuated cell recruitment, cytokine release and AHR. Conclusion MIF and HIF-1a levels are elevated in COPD BAL macrophages and inhibition of MIF function blocks corticosteroid-insensitive lung inflammation and AHR. Inhibition of MIF may provide a novel anti-inflammatory approach in COPD.
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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.
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2016 |
Gold MJ, Hiebert PR, Park HY, Stefanowicz D, Le A, Starkey MR, et al., 'Mucosal production of uric acid by airway epithelial cells contributes to particulate matter-induced allergic sensitization', Mucosal Immunology, 9 809-820 (2016) [C1] Exposure to particulate matter (PM), a major component of air pollution, contributes to increased morbidity and mortality worldwide. PM induces innate immune responses and contrib... [more] Exposure to particulate matter (PM), a major component of air pollution, contributes to increased morbidity and mortality worldwide. PM induces innate immune responses and contributes to allergic sensitization, although the mechanisms governing this process remain unclear. Lung mucosal uric acid has also been linked to allergic sensitization. The links among PM exposure, uric acid, and allergic sensitization remain unexplored. We therefore investigated the mechanisms behind PM-induced allergic sensitization in the context of lung mucosal uric acid. PM 10 and house dust mite exposure selectively induced lung mucosal uric acid production and secretion in vivo, which did not occur with other challenges (lipopolysaccharide, virus, bacteria, or inflammatory/fibrotic stimuli). PM 10 -induced uric acid mediates allergic sensitization and augments antigen-specific T-cell proliferation, which is inhibited by uricase. We then demonstrate that human airway epithelial cells secrete uric acid basally and after stimulation through a previously unidentified mucosal secretion system. Our work discovers a previously unknown mechanism of air pollution-induced, uric acid-mediated, allergic sensitization that may be important in the pathogenesis of asthma.
|
Nova | |||||||||
2016 |
Starkey MR, Nguyen DH, Brown AC, Essilfie AT, Kim RY, Yagita H, et al., 'PD-L1 Promotes Early-life Chlamydia Respiratory Infection-induced Severe Allergic Airway Disease.', American journal of respiratory cell and molecular biology, (2016) [C1]
|
Nova | |||||||||
2015 |
Essilfie A, Horvat JC, Kim RY, Mayall JR, Pinkerton JW, Beckett EL, et al., 'Macrolide therapy suppresses key features of experimental steroid-sensitive and steroid-insensitive asthma', Thorax Journal, 70 458-467 (2015) [C1]
|
Nova | |||||||||
2015 |
Hsu ACY, Starkey MR, Hanish I, Parsons K, Haw TJ, Howland LJ, et al., 'Targeting PI3K-p110a suppresses influenza virus infection in chronic obstructive pulmonary disease', American Journal of Respiratory and Critical Care Medicine, 191 1012-1023 (2015) [C1] Rationale: Chronic obstructive pulmonary disease (COPD) and influenza virus infections are major global health issues. Patients with COPD are more susceptible to infection, which ... [more] Rationale: Chronic obstructive pulmonary disease (COPD) and influenza virus infections are major global health issues. Patients with COPD are more susceptible to infection, which exacerbates their condition and increases morbidity and mortality. The mechanisms of increased susceptibility remain poorly understood, and current preventions and treatments have substantial limitations. Objectives: To characterize the mechanisms of increased susceptibility to influenza virus infection in COPD and the potential for therapeutic targeting. Methods: We used a combination of primary bronchial epithelial cells (pBECs) from COPD and healthy control subjects, a mouse model of cigarette smoke-induced experimental COPD, and influenza infection. The role of the phosphoinositide-3-kinase (PI3K) pathway was characterized using molecular methods, and its potential for targeting assessed using inhibitors. Measurements and Main Results: COPDpBECs were susceptible to increased viral entry and replication. Infected mice with experimental COPD also had more severe infection (increased viral titer and pulmonary inflammation, and compromised lung function). These processes were associated with impaired antiviral immunity, reduced retinoic acid-inducible gene-I, and IFN/cytokine and chemokine responses. Increased PI3K-p110a levels and activity inCOPDpBECs and/or mice were responsible for increased infection and reduced antiviral responses. Global PI3K, specific therapeutic p110a inhibitors, or exogenous IFN-b restored protective antiviral responses, suppressed infection, and improved lung function. Conclusions: The increased susceptibility of individuals with COPD to influenza likely results from impaired antiviral responses, which are mediated by increased PI3K-p110a activity. This pathway may be targeted therapeutically in COPD, or in healthy individuals, during seasonal or pandemic outbreaks to prevent and/or treat influenza.
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Nova | |||||||||
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]
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Nova | |||||||||
2014 |
Hansbro PM, Starkey MR, Mattes J, Horvat JC, 'Pulmonary immunity during respiratory infections in early life and the development of severe asthma', Annals of the American Thoracic Society, 11 S297-S302 (2014) [C1] Asthma affects 10% of the population in Westernized countries, being most common in children. It is a heterogeneous condition characterized by chronic allergic airway inflammation... [more] Asthma affects 10% of the population in Westernized countries, being most common in children. It is a heterogeneous condition characterized by chronic allergic airway inflammation, mucus hypersecretion, and airway hyperresponsiveness (AHR) to normally innocuous antigens. Combination therapies with inhaled corticosteroids and bronchodilators effectively manage mild to moderate asthma, but there are no cures, and patients with severe asthma do not respond to these treatments. The inception of asthma is linked to respiratory viral (respiratory syncytial virus, rhinovirus) and bacterial (Chlamydia, Mycoplasma) infections. The examination of mouse models of early-life infections and allergic airway disease (AAD) provides valuable insights into the mechanisms of disease inception that may lead to the development of more effective therapeutics. For example, early-life, but not adult, Chlamydia respiratory infections in mice permanently modify immunity and lung physiology. This increases the severity of AAD by promoting IL-13 expression, mucus hypersecretion, and AHR. We have identified novel roles for tumor necrosis factor-related apoptosisinducing ligand (TRAIL) and IL-13 in promoting infection-induced pathology in early life and subsequent chronic lung disease. Genetic deletion of TRAIL or IL-13 variously protected against neonatal infection-induced inflammation, mucus hypersecretion, altered lung structure, AHR, and impaired lung function. Therapeutic neutralization of these factors prevented infection-induced severe AAD. Other novel mechanisms and avenues for intervention are also being explored. Such studies indicate the immunological mechanisms that may underpin the association between early-life respiratory infections and the development of more severe asthma and may facilitate the development of tailored preventions and treatments.
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Nova | |||||||||
2013 |
Starkey MR, Nguyen DH, Kim RY, Nair PM, Brown AC, Essifie A-T, et al., 'Programming of the Lung in Early Life by Bacterial Infections Predisposes to Chronic Respiratory Disease', CLINICAL OBSTETRICS AND GYNECOLOGY, 56 566-576 (2013) [C1]
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2013 |
Hansbro PM, Scott GV, Essilfie A-T, Kim RY, Starkey MR, Nguyen D, et al., 'Th2 cytokine antagonists: Potential treatments for severe asthma', Expert Opinion on Investigational Drugs, 22 49-69 (2013) [C1]
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Nova | |||||||||
2013 |
Starkey MR, Jarnicki AG, Essilfie A-T, Gellatly SL, Kim RY, Brown AC, et al., 'Murine models of infectious exacerbations of airway inflammation', CURRENT OPINION IN PHARMACOLOGY, 13 337-344 (2013) [C1]
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2013 |
Starkey MR, Essilfie A-T, Horvat JC, Kim RY, Nguyen DH, Beagley KW, et al., 'Constitutive production of IL-13 promotes early-life Chlamydia respiratory infection and allergic airway disease', Mucosal Immunology, 6 569-579 (2013) [C1]
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Nova | |||||||||
2012 |
Beckett EL, Phipps S, Starkey MR, Horvat JC, Beagley KW, Foster PS, Hansbro PM, 'TLR2, but not TLR4, is required for effective host defence against chlamydia respiratory tract infection in early life', PLOS One, 7 (2012) [C1]
|
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2012 |
Starkey MR, Kim RY, Beckett EL, Schilter HC, Shim D, Essilfie A-T, et al., 'Chlamydia muridarum lung infection in infants alters hematopoietic cells to promote allergic airway disease in mice', PLoS One, 7 (2012) [C1]
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2012 |
Hansbro PM, Starkey MR, Kim RY, Stevens RL, Foster PS, Horvat JC, 'Programming of the lung by early-life infection', Journal of Developmental Origins of Health and Disease, 3 153-158 (2012) [C1]
|
Nova | |||||||||
2011 |
Preston JA, Thorburn AN, Starkey MR, Beckett EL, Horvat JC, Wade MA, et al., 'Streptococcus pneumoniae infection suppresses allergic airways disease by inducing regulatory T-cells', European Respiratory Journal, 37 53-64 (2011) [C1]
|
Nova | |||||||||
2010 |
Horvat JC, Starkey MR, Kim RY, Beagley KW, Preston JA, Gibson PG, et al., 'Chlamydial respiratory infection during allergen sensitization drives neutrophilic allergic airways disease', Journal of Immunology, 184 4159-4169 (2010) [C1]
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Nova | |||||||||
2010 |
Horvat JC, Starkey MR, Kim RY, Phipps S, Gibson PG, Beagley KW, et al., 'Early-life chlamydial lung infection enhances allergic airways disease through age-dependent differences in immunopathology', Journal of Allergy and Clinical Immunology, 125 617-625 (2010) [C1]
|
Nova | |||||||||
2010 |
Starkey MR, Horvat JC, Kim RY, Hansbro PM, 'Reply', Journal of Allergy and Clinical Immunology, 125 1415 (2010) [C3]
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Show 71 more journal articles |
Conference (73 outputs)
Year | Citation | Altmetrics | Link | ||||||||
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2022 | Bhatt N, Anderson C, Nguyen T, Rodriguez G, Burgio G, Jiang S, et al., 'ALPHA LIPOIC ACID THERAPY IS EFFECTIVE IN A PERSONALIZED MOUSE MODEL OF CYSTINURIA', NEPHROLOGY (2022) | ||||||||||
2021 |
Mayall JR, Hsu AC-Y, Horvat JC, Daly K, Chevalier A, Gomez HM, et al., 'Interferon-epsilon promotes susceptibility to influenza A and associated disease.', Online (2021)
|
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2021 |
Mayall J, Hsu A, Horvat J, Daly K, Chevalier A, Gomez H, et al., 'INTERFERON-EPSILON PROMOTES SUSCEPTIBILITY TO INFLUENZA A AND ASSOCIATED DISEASE', RESPIROLOGY (2021)
|
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2016 |
To E, Luong R, Halls M, Reading P, King P, Chan C, et al., 'NOX2 oxidase expressed in endosomes exacerbates influenza pathogenicity', EUROPEAN RESPIRATORY JOURNAL (2016)
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2015 |
Kim R, Horvat J, Pinkerton J, Starkey M, Essilfie A, Mayall J, et al., 'INFECTION-INDUCED MICRORNA-21 DRIVES SEVERE, STEROID-INSENSITIVE EXPERIMENTAL ASTHMA BY AMPLIFYING PI3K-MEDIATED SUPPRESSION OF HDAC2', RESPIROLOGY, Queensland, AUSTRALIA (2015) [E3]
|
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2015 |
Hansbro P, Kim R, Pinkerton J, Starkey M, Essilfie A-T, Mayall J, et al., 'MicroRNA-21 drives severe, steroid-insensitive experimental asthma by amplifying PI3K-mediated suppression of HDAC2', JOURNAL OF IMMUNOLOGY, New Orleans, LA (2015)
|
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2015 |
Essilfie A-T, Horvat J, Kim R, Mayall J, Pinkerton J, Beckett E, et al., 'Macrolide therapy suppresses key features of experimental steroid-sensitive and steroid insensitive asthma', JOURNAL OF IMMUNOLOGY, New Orleans, LA (2015)
|
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2015 |
Hansbro P, Haw T, Nair P, Hanish I, Nguyen D, Liu G, et al., 'Tumour necrosis factor-related apoptosis inducing ligand promotes the development of experimental chronic obstructive pulmonary disease', JOURNAL OF IMMUNOLOGY, New Orleans, LA (2015)
|
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2015 |
Hansbro P, Mayall J, Mangan N, Starkey M, Kim R, Hertzog P, Horvat J, 'Role of NK cells in IFN-epsilon-mediated protection against female reproductive tract infection', JOURNAL OF IMMUNOLOGY, New Orleans, LA (2015)
|
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2015 |
Hansbro PM, Kim RY, Pinkerton JW, Starkey MR, Essilfie AT, Mayall JR, et al., 'Infection-Induced Microrna-21 Drives Severe, Steroid-Insensitive Experimental Asthma By Amplifying PhosphoINOSitide-3-Kinase (pi3k)-Mediated Suppression Of Histone Deacetylase (hdac)2', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Denver, CO (2015)
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2014 |
Hansbro PM, Horvat JC, Kim RY, Mayall JR, Pinkerton JW, Essilfie A-T, et al., 'Antioxidant Treatment Suppresses The Progression Of Early-Life Infection-Induced Severe Asthma And Pathology In Later-Life', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2014)
|
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2014 |
Starkey M, Hanish I, Dua K, Nair P, Haw T, Hsu A, et al., 'Interleukin-13 predisposes mice to more severe influenza infection by suppressing interferon responses and activating microRNA-21/PI3K', CYTOKINE, Melbourne, AUSTRALIA (2014) [E3]
|
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2014 |
Horvat J, Kim R, Mayall J, Pinkerton J, Starkey M, Essilfie A, et al., 'ANTIOXIDANT-BASED THERAPY FOR THE SUPPRESSION OF EARLY- LIFE INFECTION-INDUCED SEVERE ASTHMA', RESPIROLOGY (2014) [E3]
|
Nova | |||||||||
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]
|
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2014 |
Starkey MR, Hanish I, Dua K, Hsu A, Monogar P, Foster PS, et al., 'Interleukin-13 Predisposes Mice To More Severe Influenza Infection And Exacerbated Allergic Airways Disease', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2014)
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2013 |
Hansbro PM, Horvat JC, Essilfie A-T, Kim RY, Mayall J, Starkey MR, et al., 'Immunomodulatory Effects Of Macrolide Treatment On Experimental Models Of Steroid-Sensitive And Steroid-Resistant Asthma', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2013)
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2013 |
Kim RY, Horvat JC, Starkey MR, Essilfie A, Foster PS, Hansbro PM, 'Inhibition Of Early-Life Chlamydia Lung Infection-Induced Micrornas Prevents Infection-Induced Lung Pathologies In Later Life', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2013)
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2013 |
Kim RY, Horvat JC, Starkey MR, Essilfie A-T, Foster PS, Hansbro PM, 'MICRORNA INHIBITION IN NEONATAL CHLAMYDIA LUNG INFECTION PREVENTS INFECTION-INDUCED LUNG PATHOLOGY IN LATER LIFE', RESPIROLOGY (2013) [E3]
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2013 |
Horvat JC, Essilfie A-T, Kim RY, Mayall JR, Starkey MR, Beckett EL, et al., 'MACROLIDES SUPPRESS KEY FEATURES OF EXPERIMENTAL STEROID-SENSITIVE AND STEROID-RESISTANT ASTHMA', RESPIROLOGY (2013) [E3]
|
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2012 |
Horvat JC, Essilfie A-T, Kim RY, Mayall JR, Starkey MR, Beckett EL, et al., 'Efficacy of antibiotic-based therapeutic strategies for the treatment of infection-induced, steroid-resistant allergic airways disease', Respirology, Canberra, ACT (2012) [E3]
|
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2012 |
Starkey MR, Kim RY, Horvat JC, Essilfie A-T, Beagley KW, Mattes J, et al., 'Constitutive IL-13 promotes respiratory chlamydial infection-induced chronic airway hyperresponsiveness', Respirology, Canberra, ACT (2012) [E3]
|
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2009 |
Hansbro PM, Starkey MR, Horvat JC, Kim RY, Phipps S, Gibson PG, Foster PS, 'Early life chlamydial infection enhances allergic airways disease through age-dependent differences in immunopathology', Journal of Immunology, Seattle, WASH. (2009) [E3]
|
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2009 |
Horvat JC, Starkey MR, Beagley KW, Gibson PG, Foster PS, Hansbro PM, 'Chlamydial respiratory infection predisposes to neutrophil dominated allergic airways disease (AAD)', Journal of Immunology, Seattle, WASH. (2009) [E3]
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2009 |
Horvat JC, Starkey MR, Beagley KW, Preston JA, Gibson PG, Foster PS, Hansbro PM, 'Neutrophil influx during chlamydial lung infection determines the phenotype of allergic airways disease (AAD)', Respirology, Darwin, NT (2009) [E3]
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2009 |
Starkey MR, Horvat JC, Kim RY, Phipps S, Gibson PG, Beagley KW, et al., 'Early life chlamydial lung infection enhances allergic airways disease through age-dependent differences in immunopathology', Respirology, Darwin, NT (2009) [E3]
|
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2008 |
Starkey MR, Horvat JC, Kim RY, Phipps S, Gibson PG, Beagley KW, et al., 'Early life chlamydial lung infection enhances allergic airways disease through age-dependent differences in immunopathology', Australasian Society for Immunology 38th Annual Scientific Meeting: Delegate Book, Canberra, ACT (2008) [E3]
|
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Show 70 more conferences |
Preprint (2 outputs)
Year | Citation | Altmetrics | Link | |||||
---|---|---|---|---|---|---|---|---|
2020 |
Bhatt N, Deshpande A, Jones-Freeman B, Jiang S, Starkey M, 'Intervention strategies for cystinuria: A systematic review (2020)
|
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2020 |
Loering S, Cameron G, Bhatt N, Belz G, Foster P, Hansbro P, Starkey M, 'Differences in pulmonary innate lymphoid cells are dependent on mouse age, sex and strain (2020)
|
Grants and Funding
Summary
Number of grants | 22 |
---|---|
Total funding | $1,257,843 |
Click on a grant title below to expand the full details for that specific grant.
20193 grants / $245,717
Understanding how group 2 innate lymphoid cells in early-life regulate postnatal lung development and susceptibility to chronic respiratory diseases$195,717
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Doctor Malcolm Starkey |
Scheme | Project Grant |
Role | Lead |
Funding Start | 2019 |
Funding Finish | 2021 |
GNo | G1800058 |
Type Of Funding | C1100 - Aust Competitive - NHMRC |
Category | 1100 |
UON | Y |
Can we improve the management of bladder dysfunction and chronic recurrent urinary tract infections in children through manipulation of the fecal and urinary microbiota: a pilot study$25,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Doctor Aniruddh Deshpande, Associate Professor Adam Collison, Doctor Malcolm Starkey |
Scheme | Project Grant |
Role | Lead |
Funding Start | 2019 |
Funding Finish | 2019 |
GNo | G1900370 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
Repurposing emerging immunotherapies to treat antibiotic resistant urinary tract infections$25,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Doctor Malcolm Starkey |
Scheme | Project Grant |
Role | Lead |
Funding Start | 2019 |
Funding Finish | 2019 |
GNo | G1901401 |
Type Of Funding | C3200 – Aust Not-for Profit |
Category | 3200 |
UON | Y |
20184 grants / $131,000
Genetic modelling to advance kidney stone and cystinuria treatments$76,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Doctor Malcolm Starkey, Doctor Aniruddh Deshpande, Professor Phil Hansbro, Dr Simon Jiang |
Scheme | Project Grant |
Role | Lead |
Funding Start | 2018 |
Funding Finish | 2020 |
GNo | G1800435 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
Immunological mechanisms in the primary prevention of asthma$25,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Associate Professor Adam Collison, Professor Joerg Mattes, Doctor Malcolm Starkey |
Scheme | Project Grant |
Role | Investigator |
Funding Start | 2018 |
Funding Finish | 2018 |
GNo | G1801259 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
Understanding how group 2 innate lymphoid cells in early-life regulate postnatal lung development and susceptibility to chronic lung diseases$20,000
Funding body: Thoracic Society of Australia and New Zealand
Funding body | Thoracic Society of Australia and New Zealand |
---|---|
Project Team | Doctor Malcolm Starkey, Professor Phil Hansbro |
Scheme | Lungs for Life Research Award |
Role | Lead |
Funding Start | 2018 |
Funding Finish | 2018 |
GNo | G1800627 |
Type Of Funding | C3200 – Aust Not-for Profit |
Category | 3200 |
UON | Y |
Understanding how Type 2 Innate Lymphoid Cells in Ealry -Life Regulate Postnatal Lung Development and Susceptibility to Chronic Lung Diseases$10,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Doctor Malcolm Starkey, Ms Svenja Loering |
Scheme | Greaves Family Postgraduate Top Up Scholarship in Medical Research |
Role | Lead |
Funding Start | 2018 |
Funding Finish | 2018 |
GNo | G1801323 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
20174 grants / $431,152
Understanding how innate lymphoid cells regulate mammalian lung development$390,307
Funding body: ARC (Australian Research Council)
Funding body | ARC (Australian Research Council) |
---|---|
Project Team | Doctor Malcolm Starkey |
Scheme | Discovery Early Career Researcher Award (DECRA) |
Role | Lead |
Funding Start | 2017 |
Funding Finish | 2019 |
GNo | G1600344 |
Type Of Funding | Aust Competitive - Commonwealth |
Category | 1CS |
UON | Y |
Understanding how immune cells repair the kidney$20,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Doctor Malcolm Starkey, Dr Aniruddh Deshpande |
Scheme | Project Grant |
Role | Lead |
Funding Start | 2017 |
Funding Finish | 2017 |
GNo | G1700006 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
DVC(RI) Research Support for DECRA (DE17) $5k pa for 3 yrs (2017,2018 & 2019) $10,845
Funding body: University of Newcastle
Funding body | University of Newcastle |
---|---|
Project Team | Doctor Malcolm Starkey |
Scheme | DECRA Support |
Role | Lead |
Funding Start | 2017 |
Funding Finish | 2019 |
GNo | G1701000 |
Type Of Funding | Internal |
Category | INTE |
UON | Y |
Countess II FL$10,000
Funding body: NSW Ministry of Health
Funding body | NSW Ministry of Health |
---|---|
Project Team | Doctor Malcolm Starkey, Associate Professor Adam Collison, Doctor Hock Tay, Doctor Aniruddh Deshpande, Doctor Gang Liu, Doctor Jemma Mayall |
Scheme | Medical Research Support Program (MRSP) |
Role | Lead |
Funding Start | 2017 |
Funding Finish | 2017 |
GNo | G1701221 |
Type Of Funding | C2400 – Aust StateTerritoryLocal – Other |
Category | 2400 |
UON | Y |
20154 grants / $99,827
Nose only inhalation smoke exposure system for mice$54,698
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Professor Phil Hansbro, Professor Paul Foster, Professor Jay Horvat, Doctor Janet Bristow, Doctor Malcolm Starkey, Doctor Rebecca Vanders, University Staff |
Scheme | Equipment Grant |
Role | Investigator |
Funding Start | 2015 |
Funding Finish | 2015 |
GNo | G1501551 |
Type Of Funding | Other Public Sector - Commonwealth |
Category | 2OPC |
UON | Y |
Early-life infections and the development of chronic disease$28,129
Funding body: Klosterfrau Healthcare Group
Funding body | Klosterfrau Healthcare Group |
---|---|
Project Team | Doctor Malcolm Starkey |
Scheme | Klosterfrau Research Grant |
Role | Lead |
Funding Start | 2015 |
Funding Finish | 2015 |
GNo | G1500307 |
Type Of Funding | C3400 – International For Profit |
Category | 3400 |
UON | Y |
Understanding how lung infections in childhood promote the development of chronic lung diseases in later life$15,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Doctor Malcolm Starkey |
Scheme | Project Grant |
Role | Lead |
Funding Start | 2015 |
Funding Finish | 2015 |
GNo | G1501367 |
Type Of Funding | Grant - Aust Non Government |
Category | 3AFG |
UON | Y |
European Congress Immunology, Austria 6-9 September 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 Malcolm Starkey |
Scheme | Travel Grant |
Role | Lead |
Funding Start | 2015 |
Funding Finish | 2015 |
GNo | G1500847 |
Type Of Funding | Internal |
Category | INTE |
UON | Y |
20144 grants / $326,147
Understanding how early-life respiratory infections promote chronic lung diseases$278,581
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Doctor Malcolm Starkey |
Scheme | Early Career Fellowships |
Role | Lead |
Funding Start | 2014 |
Funding Finish | 2017 |
GNo | G1300678 |
Type Of Funding | Aust Competitive - Commonwealth |
Category | 1CS |
UON | Y |
Miltenyi Biotec GentleMACS Octo Dissociator with Heaters $23,566
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Professor Phil Hansbro, Professor Paul Foster, Professor Darryl Knight, Professor Dirk Van Helden, Professor Joerg Mattes, Professor Jodie Simpson, Professor Lisa Wood, Prof LIZ Milward, Dr NATHAN Bartlett, Professor Simon Keely, Doctor Steven Maltby, Doctor Andrew Jarnicki, Doctor Malcolm Starkey, Associate Professor 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 |
Identification of novel therapeutic targets for Chronic Obstructive Pulmonary Disease$22,000
Funding body: Rebecca L Cooper Medical Research Foundation Ltd
Funding body | Rebecca L Cooper Medical Research Foundation Ltd |
---|---|
Project Team | Doctor Malcolm Starkey |
Scheme | Research Grant |
Role | Lead |
Funding Start | 2014 |
Funding Finish | 2014 |
GNo | G1301214 |
Type Of Funding | Grant - Aust Non Government |
Category | 3AFG |
UON | Y |
American Thoracic Society Annual Meeting, San Diego USA, 16-21 May 2014$2,000
Funding body: University of Newcastle - Faculty of Health and Medicine
Funding body | University of Newcastle - Faculty of Health and Medicine |
---|---|
Project Team | Doctor Malcolm Starkey |
Scheme | Travel Grant |
Role | Lead |
Funding Start | 2014 |
Funding Finish | 2014 |
GNo | G1400304 |
Type Of Funding | Internal |
Category | INTE |
UON | Y |
20132 grants / $20,000
HMRI Exchange Visit Travel Award 2012$10,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Doctor Malcolm Starkey |
Scheme | Project Grant |
Role | Lead |
Funding Start | 2013 |
Funding Finish | 2013 |
GNo | G1300228 |
Type Of Funding | Contract - Aust Non Government |
Category | 3AFC |
UON | Y |
Role of the transcriptional co-activator p300 in resetting epithelial differentiation: A potential pathway involved in asthma prevention and therapy$10,000
Funding body: University of Newcastle
Funding body | University of Newcastle |
---|---|
Project Team | Doctor Fatemeh Moheimani, Professor Darryl Knight, Ms Kirsty Wark, Doctor Alan Hsu, Doctor Malcolm Starkey |
Scheme | Early Career Researcher Grant |
Role | Investigator |
Funding Start | 2013 |
Funding Finish | 2013 |
GNo | G1301174 |
Type Of Funding | Internal |
Category | INTE |
UON | Y |
20121 grants / $4,000
PULSE Education Prize$4,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Doctor Malcolm Starkey |
Scheme | PULSE Education Prize |
Role | Lead |
Funding Start | 2012 |
Funding Finish | 2012 |
GNo | G1200107 |
Type Of Funding | Scheme excluded from IGS |
Category | EXCL |
UON | Y |
Research Supervision
Number of supervisions
Current Supervision
Commenced | Level of Study | Research Title | Program | Supervisor Type |
---|---|---|---|---|
2022 | Masters | Improving The Diagnosis And Management Of Chronic And Recurrent Urinary Tract Infection In Children | M Philosophy(Surgical Science), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2019 | Honours | Understanding the role of mucosal cytokines in urinary tract infections | Microbiology, Faculty of Health and Medicine, The University of Newcastle | Principal Supervisor |
Past Supervision
Year | Level of Study | Research Title | Program | Supervisor Type |
---|---|---|---|---|
2024 | PhD | Understanding the Pathogenesis of Cystinuria | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2023 | PhD | Childhood Hypospadias: Evaluating the Long-term Outcomes and Revisiting the Ideal Model of Care | PhD (Surgical Science), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2023 | PhD | Extracellular Matrix Protein 1 as a Mediator of Inflammation-to-Fibrosis Progression after Myocardial Infarction | PhD (Medicine), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2022 | PhD | Understanding How Group 2 Innate Lymphoid Cells in Early Life Regulate Postnatal Lung Development and Susceptibility to Chronic Lung Diseases | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2022 | Masters | Pharmacotherapy and Bladder Function in Children: Effects of Medications for Behavioural Disorders, Exploring New Biomarkers and Evaluating the Role of Alpha Blockers in Treating Functional Daytime Incontinence | M Philosophy(Surgical Science), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2021 | PhD | Understanding the Role of Group 2 Innate Lymphoid Cells and Mucosal Cytokines in Urinary Tract Injury and Infection | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2020 | PhD | Dietary Intervention to Reduce Exacerbation in Children with Asthma | PhD (Nutritional Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2020 | PhD | Cigarette Smoke Exposure During Pregnancy and its Effect on the Respiratory Health of Offspring | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2019 | PhD | Investigating the Mechanisms that Underpin Early-Life Chlamydia Respiratory Infection-Induced Chronic Lung Disease Using a Neonatal C. Muridarum Mouse Model | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2018 | PhD | Investigation of the Pathogenesis of Influenza Infection in Asthma and COPD; Potential Therapeutic Interventions | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2016 | PhD | Investigation of Pathogenesis of Chronic Obstructive Pulmonary Disease | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2016 | PhD | Immunoregulatory Therapies for Inflammatory Diseases | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2015 | PhD | Mechanisms of Increased Susceptibility to Influenza Infection in Mouse Models of Chronic Lung Diseases | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
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 | 135 | |
United Kingdom | 26 | |
United States | 21 | |
Canada | 10 | |
Japan | 9 | |
More... |
News
News • 12 Dec 2018
NHMRC awards $12.4 million to 14 Newcastle projects
The National Health and Medical Research Council (NHMRC) has awarded the University of Newcastle more than $12.4 million to support 14 projects that are aiming to solve some of the world’s most critical health problems and improve the lives of millions of Australians.
News • 1 Nov 2016
Australian Research Council Funding Success
The University of Newcastle (UON) has been successfully awarded over $5.7 million in 2016 Australian Research Council (ARC) funding for Discovery Projects, Future Fellowships and Discovery Early Career Researcher Awards.
News • 7 Sep 2016
UON researchers shine in a glittering field of finalists
The University of Newcastle (UON) Alumni Awards Finalists have been announced, and we are delighted to see a broad range of UON researchers represented in the outstanding field.
News • 6 Mar 2015
Rising respiratory researcher
One of Europe's premier international prizes for emerging respiratory researchers has been awarded to Dr Malcolm Starkey from the University of Newcastle and HMRI's VIVA (Viruses, Infections/Immunity, Vaccines and Asthma) Program.
Dr Malcolm Starkey
Position
Honorary Senior Lecturer
School of Biomedical Sciences and Pharmacy
College of Health, Medicine and Wellbeing
Focus area
Immunology and Microbiology
Contact Details
malcolm.starkey@newcastle.edu.au | |
Phone | (02) 40420204 |
Links |
Twitter Personal webpage |
Office
Room | W2-106 Level 2 East |
---|---|
Building | HMRI Building |
Location | John Hunter Hospital New Lambton Heights , |