Professor Jay Horvat
Professor
School of Biomedical Sciences and Pharmacy (Immunology and Microbiology)
- Email:jay.horvat@newcastle.edu.au
- Phone:(02) 40 420220
Experimental models of disease
Dr Jay Horvat's preclinical research is cementing a scientific, nuanced understanding of our bodies' harmful and helpful immunological processes
Dr Jay Horvat does his homework. He's using novel experimental models to fact check and fault-find, taking clinical observations and recapitulating them in smaller simulations to dissect and study the intricate architecture of multiple illnesses. Informing the development of innovative and preventative therapeutic treatments, this committed researcher stresses it's the endgame that's important.
"The whole point is to discover molecular mechanisms in experimental models of disease that might similarly be occurring in human patients," he explains.
"This allows us to find new therapeutic targets for the development of treatment strategies that will hopefully translate into improved clinical outcomes for patients with a variety of diseases."
Spanning the microbiological, immunological and pharmacological fields, Jay's work has a particular emphasis on illustrating the roles played by bacteria and viruses in the pathogenesis of acute inflammatory conditions. Mindful of the profound economics of chronic diseases, particularly those with ill-defined triggers, variable clinical courses and not-yet-understood symptoms, this energetic investigator's research is also serving to help construct a "big picture."
"Infection-induced illnesses still cause immense mortality and place an enormous burden on healthcare systems," Jay notes.
"This leads to unsustainable personal and societal costs."
Joining the dots
Jay started his research career with a PhD at the University of Newcastle in 2004. Under the leadership of Professor Phil Hansbro, the four-year probe sought to solidify links between respiratory chlamydia and severe asthma.
"The latter is a major unmet clinical need," he affirms.
"Patients tend to be insensitive to anti-inflammatory steroid therapies so they're usually on higher doses of medications, which could have long-term negative effects."
"Patients are in and out of hospital more often and experience more frequent and extreme exacerbations too."
"They have a lower quality of life."
Appreciating the significance of these health and social impacts, Jay looked to identify how and why severe asthma develops both early on and later in life. He also aimed to confirm hypotheses that major infections drive the disease's most acute forms.
"We found that having a Chlamydia lung infection as either a neonatal or an infant leads to severe changes in lung function as well as more severe asthma," Jay reveals.
"The neonatal infection, in particular, leads to a form of disease that resembles emphysema."
Additionally providing evidence for the existence of a phenotype switch in adults who are infected while they have asthma, Jay's doctoral research highlighted a new association between a different series of immune responses and severe, steroid-insensitive asthma.
"Eosinophils have been classically aligned with asthma," he says.
"They come into the lung during an allergic flare-up and release a variety of inflammatory mediators that can cause you to have an asthma attack."
"If you get certain infections, however, you may get neutrophils coming into the lung instead."
"The processes that drive this type of inflammation are not as easily treated."
"So the infection is causing a shift from a type of immune response that is able to be suppressed by steroids to one that is not."
Better breathing
Jay has continued collaborating with Phil Hansbro post-PhD, actively participating in a number of other asthma projects at the Hunter Medical Research Institute. An extension of his earlier work, these studies explore several bacterial and viral infections and their ties to the disease's more severe forms.
"We've shown that both Chlamydia and Haemophilus influenzae infections drive a neutrophilic subtype of asthma and that influenza and respiratory syncytial virus do not," the senior lecturer states.
"All four, however, similarly drive inflammation and lung function changes that cannot be treated with steroids."
"So we've got four infections doing slightly different things but having this universal effect of driving steroid-resistant inflammation and airway side responsiveness."
Simultaneously identifying a handful of cytokines associated with severe asthma, Jay's examination operates – and succeeds – on the proviso that if you can target a critical factor, you can meaningfully treat disease.
"Cells produce cytokines, which are basically signaling molecules that link cells up and allow them to talk to each other," he clarifies.
"They come out of the lung during an inflammatory response and tell the systemic immune response to mobilise and bring certain cells into the lung as well."
"Interleukin-1 beta is one we've found to be involved in this process."
"It's also one that's able to be depleted with antibodies, which actually suppresses the neutrophilic phenotype where steroids can't."
Looking to expand upon this knowledge, Jay's laboratory work focuses on molecular elements upstream of the newly discovered cytokine.
"A series of molecules, collectively called the 'inflammasome,' need to be activated in order for interleukin 1 beta to be secreted by cells," he says.
"If we intervene, we can stop its production and develop novel therapies for severe asthma."
"The same can be said about a novel micro-RNA we recently found."
In another offshoot of his doctoral research, Jay is surveying the effects of oxidative stress on the progression of infection-induced disease. Pointing to vitamin E as a viable, inexpensive therapeutic option, the ambitious academic is perhaps as cutting-edge as he is creative.
"If we can use this compound to treat severe asthma in early life, we can suppress all of the problems it causes later in life," he comments.
"It's quite exciting because vitamin E is something you can get from the local chemist or grocery store – it's already approved for general consumption."
Branching out and stepping up
A master at multitasking, Jay is currently working on some of his own independent research programs.
"Our most advanced one looks at how certain inflammatory stresses might affect Alzheimer's," he discloses.
"We're also examining the effect smoking has on neurodegenerative processes."
Jay and his team are hoping to uncover clues as to how and why the disease advances using their experimental models. They're similarly hoping to develop therapies that will stop or reverse it's progression.
"Chlamydia bacteria has been found in plaques of the brains of patients with Alzheimer's," he shares of the initial findings.
"We have extended these findings to show that infections enter the brain during our models of respiratory infection."
"So the infection can get into the brain – and if it can do this, it could be doing all sorts of things to affect the progression of Alzheimer's."
"We have also shown that cigarette smoking accelerates the number and size of the plaques in the brain."
Extending his research interests even further afield, the Hunter Medical Research Institute innovator is also collaborating with Dr Simon Keely on a novel food allergy project. Marrying Simon's experience in inflammatory bowel disease and Jay's experience with allergy; the study aims to explore and determine the effects of antibiotics on the microbiome and how this may affect immune processes in the gut that predispose to allergic sensitisation to normally harmless food protein.
"Antibiotic use has been linked with increased risk of developing food allergy," Jay explains.
"Importantly, antimicrobials wipe out bacteria throughout the body, especially the gut, and we think this influences immune responses and might predispose to allergic sensitization."
"We show, for example, that taking a five day course of common prescribed antibiotics results in some pretty interesting changes to the immune system in the gut."
"Our hypothesis is that food allergies are dramatically increasing in the developed world because we have a tendency to overtreat bacterial infections, which in turn has an effect on a healthy balanced immune system."
Infection protection
Jay is also collaborating with Professor Liz Milward on a research assignment that looks at the tricky interplay between iron, immune responses and infection in the context of lung disease.
"We want to understand how these three elements come together in the context of the lungs," he explains.
"Literature already tells us that both high and low iron can affect immune responses."
"It also tells us iron is important for bacterial replication."
Jay and Liz are linking a small number of hereditary disorders to this work, looking to identify ways of modifying immune responses through iron and, in doing so, improve treatment options for those suffering from a range of bacterial infections.
"Cystic fibrosis patients have increased levels of iron in their airways and this might be an important reason as to why they're more likely to get chronic colonisation with certain bacteria in the lungs," he acknowledges.
At the same time, Jay is also working with a University of Newcastle PhD student on an adaptation of his earlier respiratory Chlamydia research. This time exploring the role of immune responses in stopping the progression of femalereproductive tract Chlamydia infections, Jay is seeking to develop a comprehensive understanding of the pathogenesis of sexually transmissible infection (STI).
"The immune system in the female reproductive tract is different to other organs as it needs to be able to tolerate the implantation of an embryo that is genetically different from the mother," he comments.
"Consequently, much of what we know about immunity from research of other tissues does not completely apply to the female reproductive tract."
"While Chlamydia is able to be treated with antibiotics, a lot of infections are asymptomatic so you don't go to the doctor to get treated."
Jay explains that if Chlamydia is untreated, it is able to advance into the uterus and fallopian tubes and eventually become chronic. The immune responses elicited in order to protect against this chronic upper reproductive tract infection, can cause damage to the delicate tissues in the female reproductive tract, and this can result in serious problems including infertility, pelvic inflammatory disease and ectopic pregnancy.
"We are trying to identify the protective immune factors, and those that cause damage, so that we can develop improved therapeutic strategies for preventing and treating disease," he shares.
"In collaboration with researchers at Monash University we have identified a novel type 1 interferon that protects against infection in the female reproductive tract."
"We are currently working with this factor to try to come up with innovative therapies for Chlamydia."
"These might be applicable to other STIs, like human papillomavirus, herpes and HIV."
Related links
Experimental models of disease
Dr Jay Horvat’s preclinical research is cementing a scientific, nuanced understanding of our bodies’ harmful and helpful immunological processes
Career Summary
Biography
Research programs focus on;
Investigating the mechanisms of infection and high fat diet/obesity-induced, severe asthma
Investigating the role of the newly discovered interferon (IFN)-epsilon in Chlamydia-induced reproductive tract disease
Investigating the roles of infection and smoking in neurological diseases
Investigating the interplay between of iron, infection and immunity in the context of respiratory tract infections and lung disease
These research programs aim to inform novel targets for the development of improved therapeutic strategies for severe, steroid-resistant asthma, infection-associated respiratory and reproductive tract diseases and neurodegenerative diseases such as Alzheimer’s and multiple sclerosis.
Contribution to Research to Date; Infection & severe asthma: I have published a number of important studies that have significantly advanced the understanding of the immunological and pathophysiological interactions between lung infections and asthma. I showed for the first time that early-life, but not adult, infection enhances the severity of asthma in later life. I also showed that infection during asthma in adults results in the development of a phenotype resembling severe, steroid-resistant, neutrophilic asthma. I have since extended my research to investigate the mechanisms that underpin infection- and high fat diet/obesity-induced severe asthma in order to inform novel therapeutic strategies for disease.
Infection & reproductive tract disease: I have recently begun utilising my extensive experience in research of the immunobiology of Chlamydia infection to play a role in developing a successful research program that aims to understand the mechanisms of pathogenesis of Chlamydia reproductive tract and brain disease. We recently published a groundbreaking article in Science that demonstrated the role of IFN-epsilon in protecting against Chlamydia reproductive tract infection. I have also published a first author study that was the first to show that IL-13 promotes susceptibility to Chlamydia reproductive tract infections.
Continuing Research; My aim is to continue investigations of the association between infections and obesity and severe, steroid-resistant asthma and of infection-induced, reproductive tract disease. I have been awarded an NHMRC Project Grant (2013-16) to elucidate the mechanisms of and discover new treatments for steroid-resistant asthma. I am also a Chief Investigator on a NHMRC Project Grant application for funding 2014-16 that will elucidate the mechanisms IFN-epsilon mediated protection against Chlamydia-infection in the reproductive tract.
Establishing Novel Research Programs; I have begun investigating the association between infection and cigarette smoking with a number of other diseases including Alzheimer’s and other neurodegenerative disorders. I also have recently initiated a program that focusses on investigating the interplay between iron, infection and immunity in lung and the effect this has on respiratory disease.Qualifications
- Doctor of Philosophy, University of Newcastle
- Bachelor of Biomedical Sciences (Hons), University of Newcastle
Keywords
- Immunology
- Pharmaceutical Sciences
- Pharmacology
Fields of Research
Code | Description | Percentage |
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321599 | Reproductive medicine not elsewhere classified | 15 |
310799 | Microbiology not elsewhere classified | 15 |
320499 | Immunology not elsewhere classified | 70 |
Professional Experience
UON Appointment
Title | Organisation / Department |
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Professor | University of Newcastle School of Biomedical Sciences and Pharmacy Australia |
Publications
For publications that are currently unpublished or in-press, details are shown in italics.
Chapter (1 outputs)
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2021 |
Ali MK, Horvat JC, Spiekerkoetter EF, 'Targeting Molecular and Cellular Mechanisms of Pulmonary Arterial Hypertension', Targeting Cellular Signalling Pathways in Lung Diseases 407-434 (2021) Pulmonary arterial hypertension (PAH) is a devastating disease of the pulmonary circulation, characterized by pulmonary vascular remodeling leading to elevated pulmonary arterial ... [more] Pulmonary arterial hypertension (PAH) is a devastating disease of the pulmonary circulation, characterized by pulmonary vascular remodeling leading to elevated pulmonary arterial pressure, increased pulmonary vascular resistance, and right heart failure. Unfortunately, up until now, no definite cure exists for this disease. Currently available drugs focus on pulmonary vasodilation, anti-proliferation, and augmentation of endothelial function by targeting nitric oxide, endothelin, voltage-gated calcium channels, and prostacyclin signaling pathways. However, these drugs only partially improve survival and quality of life as they do not address the underlying pulmonary vascular remodeling. Over the past few years, attempts have been made to identify effective therapies that target different, antiremodeling mechanisms and signaling pathways. Targets for these therapies include genetic and epigenetic modifications, growth factors and proliferation, inflammation and immunomodulation, endothelial-mesenchymal transition, and metabolic abnormalities. In this chapter, we outline and discuss promising novel therapeutic approaches that target diverse molecular and cellular signaling mechanisms involved in PAH.
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Journal article (106 outputs)
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2024 |
Hedley KE, Cuskelly A, Callister RJ, Horvat JC, Hodgson DM, Tadros MA, 'The medulla oblongata shows a sex-specific inflammatory response to systemic neonatal lipopolysaccharide', Journal of Neuroimmunology, 389 (2024) [C1] Early life inflammation has been linked to long-term modulation of behavioural outcomes due to the central nervous system, but it is now becoming apparent it is also linked to dys... [more] Early life inflammation has been linked to long-term modulation of behavioural outcomes due to the central nervous system, but it is now becoming apparent it is also linked to dysfunction of visceral physiology. The medulla oblongata contains a number of nuclei critical for homeostasis, therefore we utilised the well-established model of neonatal lipopolysaccharide (LPS) exposure to examine the immediate and long-term impacts of systemic inflammation on the medulla oblongata. Wistar rats were injected with LPS or saline on postnatal days 3 and 5, with tissues collected on postnatal days 7 or 90 in order to assess expression of inflammatory mediators and microglial morphology in autonomic regions of the medulla oblongata. We observed a distinct sex-specific response of all measured inflammatory mediators at both ages, as well as significant neonatal sex differences in inflammatory mediators within saline groups. At both ages, microglial morphology had significant changes in branch length and soma size in a sex-specific manner in response to LPS exposure. This data not only highlights the strong sex-specific response of neonates to LPS administration, but also the significant life-long impact on the medulla oblongata and the potential altered control of visceral organs.
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2024 |
Budden KF, Shukla SD, Bowerman KL, Vaughan A, Gellatly SL, Wood DLA, et al., 'Faecal microbial transfer and complex carbohydrates mediate protection against COPD.', Gut, (2024) [C1]
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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 |
Tu X, Gomez HM, Kim RY, Brown AC, de Jong E, Galvao I, et al., 'Airway and parenchyma transcriptomics in a house dust mite model of experimental asthma', Respiratory Research, 24 (2023) [C1] Lung transcriptomics studies in asthma have provided valuable information in the whole lung context, however, deciphering the individual contributions of the airway and parenchyma... [more] Lung transcriptomics studies in asthma have provided valuable information in the whole lung context, however, deciphering the individual contributions of the airway and parenchyma in disease pathogenesis may expedite the development of novel targeted treatment strategies. In this study, we performed transcriptomics on the airway and parenchyma using a house dust mite (HDM)-induced model of experimental asthma that replicates key features of the human disease. HDM exposure increased the expression of 3,255 genes, of which 212 were uniquely increased in the airways, 856 uniquely increased in the parenchyma, and 2187 commonly increased in both compartments. Further interrogation of these genes using a combination of network and transcription factor enrichment analyses identified several transcription factors that regulate airway and/or parenchymal gene expression, including transcription factor EC (TFEC), transcription factor PU.1 (SPI1), H2.0-like homeobox (HLX), metal response element binding transcription factor-1 (MTF1) and E74-like factor 4 (ets domain transcription factor, ELF4) involved in controlling innate immune responses. We next assessed the effects of inhibiting lung SPI1 responses using commercially available DB1976 and DB2313 on key disease outcomes. We found that both compounds had no protective effects on airway inflammation, however DB2313 (8¿mg/kg) decreased mucus secreting cell number, and both DB2313 (1¿mg/kg) and DB1976 (2.5¿mg/kg and 1¿mg/kg) reduced small airway collagen deposition. Significantly, both compounds decreased airway hyperresponsiveness. This study demonstrates that SPI1 is important in HDM-induced experimental asthma and that its pharmacological inhibition reduces HDM-induced airway collagen deposition and hyperresponsiveness.
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2023 |
Vanders RL, Gomez HM, Hsu AC, Daly K, Wark PAB, Horvat JC, Hansbro PM, 'Inflammatory and antiviral responses to influenza A virus infection are dysregulated in pregnant mice with allergic airway disease.', Am J Physiol Lung Cell Mol Physiol, 325 L385-L398 (2023) [C1]
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2023 |
Beyene T, Zosky GRR, Gibson PGG, McDonald VMM, Holliday EGG, Horvat JCC, et al., 'The impact of the 2019/2020 Australian landscape fires on infant feeding and contaminants in breast milk in women with asthma', INTERNATIONAL BREASTFEEDING JOURNAL, 18 (2023) [C1]
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2023 |
Vertigan AE, Harvey ES, Beyene T, Van Buskirk J, Holliday EG, Bone SL, et al., 'Impact of Landscape Fire Smoke Exposure on Patients With Asthma With or Without Laryngeal Hypersensitivity.', The journal of allergy and clinical immunology. In practice, 11 3107-3115.e2 (2023) [C1]
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2023 |
Attia J, Horvat JC, Hunter T, Hansbro PM, Hure A, Peel R, et al., 'Persistence of Detectable Anti-Pneumococcal Antibodies 4 Years After Pneumococcal Polysaccharide Vaccination in a Randomised Controlled Trial: The Australian Study for the Prevention through Immunisation of Cardiovascular Events (AUSPICE)', Heart, Lung and Circulation, 32 1378-1385 (2023) [C1]
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2023 |
Burns GL, Potter M, Mathe A, Bruce J, Minahan K, Barnes JL, et al., 'TRAV26-2 T-Cell Receptor Expression Is Associated With Mucosal Lymphocyte Response to Wheat Proteins in Patients With Functional Dyspepsia.', Clin Transl Gastroenterol, 14 e00638 (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 |
Horvat JC, Kim RY, Weaver N, Augood C, Brown AC, Donovan C, et al., 'Characterization and inhibition of inflammasome responses in severe and non-severe asthma.', Respir Res, 24 303 (2023) [C1]
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2023 |
Scott HA, Ng SH, McLoughlin RF, Valkenborghs SR, Nair P, Brown AC, et al., 'Effect of obesity on airway and systemic inflammation in adults with asthma: a systematic review and meta-analysis.', Thorax, 78 957-965 (2023) [C1]
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2023 |
Cooper GE, Mayall J, Donovan C, Haw TJ, Budden KF, Hansbro NG, et al., 'Antiviral Responses of Tissue-resident CD49a+ Lung Natural Killer Cells Are Dysregulated in Chronic Obstructive Pulmonary Disease.', Am J Respir Crit Care Med, 207 553-565 (2023) [C1]
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2022 |
Runtsch MC, Angiari S, Hooftman A, Wadhwa R, Zhang Y, Zheng Y, et al., 'Itaconate and itaconate derivatives target JAK1 to suppress alternative activation of macrophages', Cell Metabolism, 34 487-501.e8 (2022) [C1] The Krebs cycle-derived metabolite itaconate and its derivatives suppress the inflammatory response in pro-inflammatory ¿M1¿ macrophages. However, alternatively activated ¿M2¿ mac... [more] The Krebs cycle-derived metabolite itaconate and its derivatives suppress the inflammatory response in pro-inflammatory ¿M1¿ macrophages. However, alternatively activated ¿M2¿ macrophages can take up itaconate. We therefore examined the effect of itaconate and 4-octyl itaconate (OI) on M2 macrophage activation. We demonstrate that itaconate and OI inhibit M2 polarization and metabolic remodeling. Examination of IL-4 signaling revealed inhibition of JAK1 and STAT6 phosphorylation by both itaconate and OI. JAK1 activation was also inhibited by OI in response to IL-13, interferon-ß, and interferon-¿ in macrophages and in T helper 2 (Th2) cells. Importantly, JAK1 was directly modified by itaconate derivatives at multiple residues, including cysteines 715, 816, 943, and 1130. Itaconate and OI also inhibited JAK1 kinase activity. Finally, OI treatment suppressed M2 macrophage polarization and JAK1 phosphorylation in vivo. We therefore identify itaconate and OI as JAK1 inhibitors, suggesting a new strategy to inhibit JAK1 in M2 macrophage-driven diseases.
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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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2022 |
Donovan C, Kim RY, Galvao I, Jarnicki AG, Brown AC, Jones-Freeman B, et al., 'Aim2 suppresses cigarette smoke-induced neutrophil recruitment, neutrophil caspase-1 activation and anti-Ly6G-mediated neutrophil depletion', IMMUNOLOGY AND CELL BIOLOGY, 100 235-249 (2022) [C1]
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2022 |
Beyene T, Murphy VE, Gibson PG, McDonald VM, Van Buskirk J, Holliday EG, et al., 'The impact of prolonged landscape fire smoke exposure on women with asthma in Australia', BMC Pregnancy and Childbirth, 22 (2022) [C1] Background: Little is known about the physical and mental health impact of exposure to landscape fire smoke in women with asthma. This study examined the health impacts and inform... [more] Background: Little is known about the physical and mental health impact of exposure to landscape fire smoke in women with asthma. This study examined the health impacts and information-seeking behaviours of women with asthma exposed to the 2019/2020 Australian fires, including women who were pregnant. Methods: Women with asthma were recruited from the Breathing for Life Trial in Australia. Following the landscape fire exposure period, self-reported data were collected regarding symptoms (respiratory and non-respiratory), asthma exacerbations, wellbeing, quality of life, information seeking, and landscape fire smoke exposure mitigation strategies. Participants¿ primary residential location and fixed site monitoring was used to geolocate and estimate exposure to landscape fire-related fine Particulate Matter (PM2.5). Results: The survey was completed by 81 pregnant, 70 breastfeeding and 232 non-pregnant and non-breastfeeding women with asthma. Participants had a median daily average of 17 µg/m3 PM2.5 and 105 µg/m3 peak PM2.5 exposure over the fire period (October 2019 to February 2020). Over 80% of participants reported non-respiratory and respiratory symptoms during the fire period and 41% reported persistent symptoms. Over 82% reported asthma symptoms and exacerbations of asthma during the fire period. Half the participants sought advice from a health professional for their symptoms. Most (97%) kept windows/doors shut when inside and 94% stayed indoors to minimise exposure to landscape fire smoke. Over two in five (43%) participants reported that their capacity to participate in usual activities was reduced due to prolonged smoke exposure during the fire period. Participants reported greater anxiety during the fire period than after the fire period (mean (SD) = 53(13) versus 39 (13); p < 0.001). Two in five (38%) pregnant participants reported having concerns about the effect of fire events on their pregnancy. Conclusion: Prolonged landscape fire smoke exposure during the 2019/2020 Australian fire period had a significant impact on the health and wellbeing of women with asthma, including pregnant women with asthma. This was despite most women taking actions to minimise exposure to landscape fire smoke. Effective and consistent public health messaging is needed during landscape fire events to guard the health of women with asthma.
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2022 |
Hedley KE, Callister RJ, Callister R, Horvat JC, Tadros MA, 'Alterations in brainstem respiratory centers following peripheral inflammation: A systematic review', JOURNAL OF NEUROIMMUNOLOGY, 369 (2022) [C1]
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2022 |
Vanka KS, Shukla S, Gomez HM, James C, Palanisami T, Williams K, et al., 'Understanding the pathogenesis of occupational coal and silica dust-associated lung disease', EUROPEAN RESPIRATORY REVIEW, 31 (2022) [C1]
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2022 |
Pathinayake PS, Waters DW, Nichol KS, Brown AC, Reid AT, Hsu AC-Y, et al., 'Endoplasmic reticulum-unfolded protein response signalling is altered in severe eosinophilic and neutrophilic asthma', THORAX, 77 443-451 (2022) [C1]
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2022 |
Budden KF, Gellatly SL, Vaughan A, Amorim N, Horvat JC, Hansbro NG, et al., 'Probiotic Bifidobacterium longum subsp. longum Protects against Cigarette Smoke-Induced Inflammation in Mice.', Int J Mol Sci, 24 (2022) [C1]
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2022 |
Ren S, Hansbro PM, Srikusalanukul W, Horvat JC, Hunter T, Brown AC, et al., 'Generation of cardio-protective antibodies after pneumococcal polysaccharide vaccine: Early results from a randomised controlled trial', Atherosclerosis, 346 68-74 (2022) [C1] Background and aims: Observational studies have demonstrated that the pneumococcal polysaccharide vaccine (PPV) is associated with reduced risk of cardiovascular events. This may ... [more] Background and aims: Observational studies have demonstrated that the pneumococcal polysaccharide vaccine (PPV) is associated with reduced risk of cardiovascular events. This may be mediated through IgM antibodies to OxLDL, which have previously been associated with cardioprotective effects. The Australian Study for the Prevention through Immunisation of Cardiovascular Events (AUSPICE) is a double-blind, randomised controlled trial (RCT) of PPV in preventing ischaemic events. Participants received PPV or placebo once at baseline and are being followed-up for incident fatal and non-fatal myocardial infarction or stroke over 6 years. Methods: A subgroup of participants at one centre (Canberra; n = 1,001) were evaluated at 1 month and 2 years post immunisation for changes in surrogate markers of atherosclerosis, as pre-specified secondary outcomes: high-sensitive C-reactive protein (CRP), pulse wave velocity (PWV), and carotid intima-media thickness (CIMT). In addition, 100 participants were randomly selected in each of the intervention and control groups for measurement of anti-pneumococcal antibodies (IgG, IgG2, IgM) as well as anti-OxLDL antibodies (IgG and IgM to CuOxLDL, MDA-LDL, and PC-KLH). Results: Concentrations of anti-pneumococcal IgG and IgG2 increased and remained high at 2 years in the PPV group compared to the placebo group, while IgM increased and then declined, but remained detectable, at 2 years. There were statistically significant increases in all anti-OxLDL IgM antibodies at 1 month, which were no longer detectable at 2 years; there was no increase in anti-OxLDL IgG antibodies. There were no significant changes in CRP, PWV or CIMT between the treatment groups at the 2-year follow-up. Conclusions: PPV engenders a long-lasting increase in anti-pneumococcal IgG, and to a lesser extent, IgM titres, as well as a transient increase in anti-OxLDL IgM antibodies. However, there were no detectable changes in surrogate markers of atherosclerosis at the 2-year follow-up. Long-term, prospective follow-up of clinical outcomes is continuing to assess if PPV reduces CVD events.
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2022 |
Burns GL, Bruce JK, Minahan K, Mathe A, Fairlie T, Cameron R, et al., 'Type 2 and type 17 effector cells are increased in the duodenal mucosa but not peripheral blood of patients with functional dyspepsia.', Front Immunol, 13 1051632 (2022) [C1]
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2022 |
Beyene T, Harvey ES, Van Buskirk J, McDonald VM, Jensen ME, Horvat JC, et al., ''Breathing Fire': Impact of Prolonged Bushfire Smoke Exposure in People with Severe Asthma', INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH, 19 (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 |
Moecking J, Laohamonthonkul P, Chalker K, White MJ, Harapas CR, Yu CH, et al., 'NLRP1 variant M1184V decreases inflammasome activation in the context of DPP9 inhibition and asthma severity', Journal of Allergy and Clinical Immunology, 147 2134-2145.e20 (2021) [C1] Background: NLRP1 is an innate immune sensor that can form cytoplasmic inflammasome complexes. Polymorphisms in NLRP1 are linked to asthma; however, there is currently no function... [more] Background: NLRP1 is an innate immune sensor that can form cytoplasmic inflammasome complexes. Polymorphisms in NLRP1 are linked to asthma; however, there is currently no functional or mechanistic explanation for this. Objective: We sought to clarify the role of NLRP1 in asthma pathogenesis. Methods: Results from the GALA II cohort study were used to identify a link between NLRP1 and asthma in Mexican Americans. In vitro and in vivo models for NLRP1 activation were applied to investigate the role of this inflammasome in asthma at the molecular level. Results: We document the association of an NLRP1 haplotype with asthma for which the single nucleotide polymorphism rs11651270 (M1184V) individually is the most significant. Surprisingly, M1184V increases NLRP1 activation in the context of N-terminal destabilization, but decreases NLRP1 activation on dipeptidyl peptidase 9 inhibition. In vitro studies demonstrate that M1184V increases binding to dipeptidyl peptidase 9, which can account for its inhibitory role in this context. In addition, in vivo data from a mouse model of airway inflammation reveal a protective role for NLRP1 inflammasome activation reducing eosinophilia in this setting. Conclusions: Linking our in vitro and in vivo results, we found that the NLRP1 variant M1184V reduces inflammasome activation in the context of dipeptidyl peptidase 9 inhibition and could thereby increase asthma severity. Our studies may have implications for the treatment of asthma in patients carrying this variant of NLRP1.
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2021 |
Tu X, Donovan C, Kim RY, Wark PAB, Horyat JC, Hansbro PM, 'Asthma-COPD overlap: current understanding and the utility of experimental models', EUROPEAN RESPIRATORY REVIEW, 30 (2021) [C1]
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2021 |
Barnes JL, Plank MW, Asquith K, Maltby S, Sabino LR, Kaiko GE, et al., 'T-helper 22 cells develop as a distinct lineage from Th17 cells during bacterial infection and phenotypic stability is regulated by T-bet', MUCOSAL IMMUNOLOGY, 14 1077-1087 (2021) [C1]
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2021 |
Kim RY, Sunkara KP, Bracke KR, Jarnicki AG, Donovan C, Hsu AC, et al., 'microRNA-21-mediated SATB1/S100A9/NF-kappa B axis promotes chronic obstructive pulmonary disease pathogenesis', SCIENCE TRANSLATIONAL MEDICINE, 13 (2021) [C1]
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2021 |
Goggins BJ, Minahan K, Sherwin S, Soh WS, Pryor J, Bruce J, et al., 'Pharmacological HIF-1 stabilization promotes intestinal epithelial healing through regulation of alpha-integrin expression and function', AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 320 G420-G438 (2021) [C1]
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2021 |
Lu Z, Van Eeckhoutte HP, Liu G, Nair PM, Jones B, Gillis CM, et al., 'Necroptosis Signaling Promotes Inflammation, Airway Remodeling, and Emphysema in Chronic Obstructive Pulmonary Disease', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 204 667-681 (2021) [C1]
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2021 |
Gomez HM, Pillar AL, Brown AC, Kim RY, Ali MK, Essilfie A-T, et al., 'Investigating the Links between Lower Iron Status in Pregnancy and Respiratory Disease in Offspring Using Murine Models', NUTRIENTS, 13 (2021) [C1]
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2020 |
Woods JJ, Skelding KA, Martin KL, Aryal R, Sontag E, Johnstone DM, et al., 'Assessment of evidence for or against contributions of Chlamydia pneumoniae infections to Alzheimer's disease etiology', Brain, Behavior, and Immunity, 83 22-32 (2020) [C1] Alzheimer's disease, the most common form of dementia, was first formally described in 1907 yet its etiology has remained elusive. Recent proposals that Aß peptide may be par... [more] Alzheimer's disease, the most common form of dementia, was first formally described in 1907 yet its etiology has remained elusive. Recent proposals that Aß peptide may be part of the brain immune response have revived longstanding contention about the possibility of causal relationships between brain pathogens and Alzheimer's disease. Research has focused on infectious pathogens that may colonize the brain such as herpes simplex type I. Some researchers have proposed the respiratory bacteria Chlamydia pneumoniae may also be implicated in Alzheimer's disease, however this remains controversial. This review aims to provide a balanced overview of the current evidence and its limitations and future approaches that may resolve controversies. We discuss the evidence from in vitro, animal and human studies proposed to implicate Chlamydia pneumoniae in Alzheimer's disease and other neurological conditions, the potential mechanisms by which the bacterium may contribute to pathogenesis and limitations of previous studies that may explain the inconsistencies in the literature.
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2020 |
Vidaillac C, Yong VFL, Aschtgen MS, Qu J, Yang S, Xu G, et al., 'Sex steroids induce membrane stress responses and virulence properties in pseudomonas aeruginosa', mBio, 11 1-19 (2020) [C1] Estrogen, a major female sex steroid hormone, has been shown to promote the selection of mucoid Pseudomonas aeruginosa in the airways of patients with chronic respiratory diseases... [more] Estrogen, a major female sex steroid hormone, has been shown to promote the selection of mucoid Pseudomonas aeruginosa in the airways of patients with chronic respiratory diseases, including cystic fibrosis. This results in long-term persistence, poorer clinical outcomes, and limited therapeutic options. In this study, we demonstrate that at physiological concentrations, sex steroids, including testosterone and estriol, induce membrane stress responses in P. aeruginosa. This is characterized by increased virulence and consequent inflammation and release of proinflammatory outer membrane vesicles promoting in vivo persistence of the bacteria. The steroid-induced P. aeruginosa response correlates with the molecular polarity of the hormones and membrane fluidic properties of the bacteria. This novel mechanism of interaction between sex steroids and P. aeruginosa explicates the reported increased disease severity observed in females with cystic fibrosis and provides evidence for the therapeutic potential of the modulation of sex steroids to achieve better clinical outcomes in patients with hormone-responsive strains. IMPORTANCE Molecular mechanisms by which sex steroids interact with P. aeruginosa to modulate its virulence have yet to be reported. Our work provides the first characterization of a steroid-induced membrane stress mechanism promoting P. aeruginosa virulence, which includes the release of proinflammatory outer membrane vesicles, resulting in inflammation, host tissue damage, and reduced bacterial clearance. We further demonstrate that at nanomolar (physiological) concentrations, male and female sex steroids promote virulence in clinical strains of P. aeruginosa based on their dynamic membrane fluidic properties. This work provides, for the first-time, mechanistic insight to better understand and predict the P. aeruginosa related response to sex steroids and explain the interindividual patient variability observed in respiratory diseases such as cystic fibrosis that are complicated by gender differences and chronic P. aeruginosa infection.
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2020 |
Bezerra-Santos CR, Bondarenko E, Essilfie AT, Nair PM, Horvat JC, Barbosa-Filho JM, et al., 'Cissampelos sympodialis and Warifteine Suppress Anxiety-Like Symptoms and Allergic Airway Inflammation in Acute Murine Asthma Model', REVISTA BRASILEIRA DE FARMACOGNOSIA-BRAZILIAN JOURNAL OF PHARMACOGNOSY, 30 224-232 (2020) [C1]
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2020 |
Lee JM, Mayall JR, Chevalier A, McCarthy H, Van Helden D, Hansbro PM, et al., 'Chlamydia muridarum infection differentially alters smooth muscle function in mouse uterine horn and cervix', American Journal of Physiology - Endocrinology and Metabolism, 318 E981-E994 (2020) [C1] Lee JM, Mayall JR, Chevalier A, McCarthy H, Van Helden D, Hansbro PM, Horvat JC, Jobling P. Chlamydia muridarum infection differentially alters smooth muscle function in mouse ute... [more] Lee JM, Mayall JR, Chevalier A, McCarthy H, Van Helden D, Hansbro PM, Horvat JC, Jobling P. Chlamydia muridarum infection differentially alters smooth muscle function in mouse uterine horn and cervix. Am J Physiol Endocrinol Metab 318: E981 E994, 2020. First published April 21, 2020; doi:10.1152/ajpendo.00513. 2019. Chlamydia trachomatis infection is a primary cause of reproductive tract diseases including infertility. Previous studies showed that this infection alters physiological activities in mouse oviducts. Whether this occurs in the uterus and cervix has never been investigated. This study characterized the physiological activities of the uterine horn and the cervix in a Chlamydia muridarum (Cmu)-infected mouse model at three infection time points of 7, 14, and 21 days postinfection (dpi). Cmu infection significantly decreased contractile force of spontaneous contraction in the cervix (7 and 14 dpi; P < 0.001 and P < 0.05, respectively), but this effect was not observed in the uterine horn. The responses of the uterine horn and cervix to oxytocin were significantly altered by Cmu infection at 7 dpi (P < 0.0001), but such responses were attenuated at 14 and 21 dpi. Cmu infection increased contractile force to prostaglandin (PGF2_) by 53 83% in the uterine horn. This corresponded with the increased messenger ribonucleic acid (mRNA) expression of Ptgfr that encodes for its receptor. However, Cmu infection did not affect contractions of the uterine horn and cervix to PGE2 and histamine. The mRNA expression of Otr and Ptger4 was inversely correlated with the mRNA expression of Il1b, Il6 in the uterine horn of Cmu-inoculated mice (P < 0.01 to P < 0.001), suggesting that the changes in the Otr and Ptger4 mRNA expression might be linked to the changes in inflammatory cytokines. Lastly, this study also showed a novel physiological finding of the differential response to PGE2 in mouse uterine horn and cervix.
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2020 |
Ali MK, Kim RY, Brown AC, Donovan C, Vanka KS, Mayall JR, et al., 'Critical role for iron accumulation in the pathogenesis of fibrotic lung disease', JOURNAL OF PATHOLOGY, 251 49-62 (2020) [C1]
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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 |
Pinkerton JW, Kim RY, Koeninger L, Armbruster NS, Hansbro NG, Brown AC, et al., 'Human beta-defensin-2 suppresses key features of asthma in murine models of allergic airways disease', CLINICAL AND EXPERIMENTAL ALLERGY, 51 120-131 (2020) [C1]
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2020 |
Pryor J, Burns GL, Duncanson K, Horvat JC, Walker MM, Talley NJ, Keely S, 'Functional Dyspepsia and Food: Immune Overlap with Food Sensitivity Disorders.', Current gastroenterology reports, 22 (2020) [C1]
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2019 |
Keenan CR, Iannarella N, Garnham AL, Brown AC, Kim RY, Horvat JC, et al., 'Polycomb repressive complex 2 is a critics mediator of allergic inflammation', JCI INSIGHT, 4 (2019) [C1]
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2019 |
Rutting S, Xenaki D, Malouf M, Horvat JC, Wood LG, Hansbro PM, Oliver BG, 'Short-chain fatty acids increase tnfa-induced inflammation in primary human lung mesenchymal cells through the activation of p38 mapk', American Journal of Physiology - Lung Cellular and Molecular Physiology, 316 L157-L174 (2019) [C1] Short-chain fatty acids (SCFAs), produced as by-products of dietary fiber metabolism by gut bacteria, have anti-inflammatory properties and could potentially be used for the treat... [more] Short-chain fatty acids (SCFAs), produced as by-products of dietary fiber metabolism by gut bacteria, have anti-inflammatory properties and could potentially be used for the treatment of inflammatory diseases, including asthma. The direct effects of SCFAs on inflammatory responses in primary human lung mesenchymal cells have not been assessed. We investigated whether SCFAs can protect against tumor necrosis factor (TNF) a-induced inflammation in primary human lung fibroblasts (HLFs) and airway smooth muscle (ASM) cells in vitro. HLFs and ASM cells were exposed to SCFAs, acetate (C2:0), propionate (C3:0), and butyrate (C4:0) (0.01¿25 mM) with or without TNFa, and the release of proinflammatory cytokines, IL-6, and CXCL8 was measured using ELISA. We found that none of the SCFAs suppressed TNFa-induced cytokine release. On the contrary, challenge with supraphysiological concentrations (10 ¿25 mM), as might be used therapeutically, of propionate or butyrate in combination with TNFa resulted in substantially greater IL-6 and CXCL8 release from HLFs and ASM cells than challenge with TNFa alone, demonstrating synergistic effects. In ASM cells, challenge with acetate also enhanced TNFa-induced IL-6, but not CXCL8 release. Synergistic upregulation of IL-6 and CXCL8 was mediated through the activation of free fatty acid receptor (FFAR)3, but not FFAR2. The signaling pathways involved were further examined using specific inhibitors and immunoblotting, and responses were found to be mediated through p38 MAPK signaling. This study demonstrates that proinflammatory, rather than anti-inflammatory effects of SCFAs are evident in lung mesenchymal cells.
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2019 |
B Biomed GB, Carroll G, Mathe A, Horvat J, Foster P, Walker MM, et al., 'Evidence for Local and Systemic Immune Activation in Functional Dyspepsia and the Irritable Bowel Syndrome: A Systematic Review', American Journal of Gastroenterology, 114 429-436 (2019) [C1] BACKGROUND:Subtle histopathologic features such as eosinophilia and increased mast cells have been observed in functional gastrointestinal disorders (FGIDs), including functional ... [more] BACKGROUND:Subtle histopathologic features such as eosinophilia and increased mast cells have been observed in functional gastrointestinal disorders (FGIDs), including functional dyspepsia (FD) and the irritable bowel syndrome (IBS). The mechanisms that drive recruitment of these cells to the gastrointestinal tract remain unexplained, largely due to the heterogeneity in phenotypes among patients diagnosed with such conditions. We aimed to systematically review the literature and collate the evidence for immune activation in FD and IBS, and where possible, detail the nature of activation.METHODS:Seven literature databases were searched using the keywords: 'functional gastrointestinal disorder', FGID, 'functional dyspepsia', 'non-ulcer dyspepsia', 'idiopathic dyspepsia', 'irritable bowel syndrome', IBS and 'immun*'.RESULTS:Fifty-one papers reporting discordant immune features met the selection criteria for this review. Changes in lymphocyte populations, including B and T lymphocyte numbers and activation status were reported in IBS and FD, in conjunction with duodenal eosinophilia in FD and increased colonic mast cells in IBS. Increases in circulating a4+ß7+ gut-homing T cells appear to be linked to the pathophysiology of both FD and IBS. Studies in the area are complicated by poor phenotyping of patients into subgroups and the subtle nature of the immune activity involved in FD and IBS.CONCLUSIONS:Alterations in proportions of gut-homing T lymphocytes in both FD and IBS indicate that a loss of mucosal homeostasis may drive the symptoms of FD and IBS. There is indirect evidence that Th17 responses may play a role in FGIDs, however the evidence for a Th2 immune phenotype in FD and IBS is limited. Although immune involvement is evident, large, well-characterised patient cohorts are required to elucidate the immune mechanisms driving the development of FGIDs.
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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 |
Rutting S, Zakarya R, Bozier J, Xenaki D, Horvat JC, Wood LG, et al., 'Dietary Fatty Acids Amplify Inflammatory Responses to Infection through p38 MAPK Signaling.', American journal of respiratory cell and molecular biology, 60 554-568 (2019) [C1]
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2019 |
Wood LG, Li Q, Scott HA, Rutting S, Berthon BS, Gibson PG, et al., 'Saturated fatty acids, obesity, and the nucleotide oligomerization domain-like receptor protein 3 (NLRP3) inflammasome in asthmatic patients', JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 143 305-315 (2019) [C1]
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2019 |
Wadhwa R, Dua K, Adcock IM, Horvat JC, Kim RY, Hansbro PM, 'Cellular mechanisms underlying steroid-resistant asthma.', European respiratory review : an official journal of the European Respiratory Society, 28 (2019) [C1]
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2019 |
Liu G, Cooley MA, Jarnicki AG, Borghuis T, Nair PM, Tjin G, et al., 'Fibulin-1c regulates transforming growth factor-beta activation in pulmonary tissue fibrosis', JCI INSIGHT, 4 (2019) [C1]
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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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2018 |
Mateer SW, Mathe A, Bruce J, Liu G, Maltby S, Fricker M, et al., 'IL-6 Drives Neutrophil-Mediated Pulmonary Inflammation Associated with Bacteremia in Murine Models of Colitis', American Journal of Pathology, 188 1625-1639 (2018) [C1] Inflammatory bowel disease (IBD) is associated with several immune-mediated extraintestinal manifestations. More than half of all IBD patients have some form of respiratory pathol... [more] Inflammatory bowel disease (IBD) is associated with several immune-mediated extraintestinal manifestations. More than half of all IBD patients have some form of respiratory pathology, most commonly neutrophil-mediated diseases, such as bronchiectasis and chronic bronchitis. Using murine models of colitis, we aimed to identify the immune mechanisms driving pulmonary manifestations of IBD. We found increased neutrophil numbers in lung tissue associated with the pulmonary vasculature in both trinitrobenzenesulfonic acid¿ and dextran sulfate sodium¿induced models of colitis. Analysis of systemic inflammation identified that neutrophilia was associated with bacteremia and pyrexia in animal models of colitis. We further identified IL-6 as a systemic mediator of neutrophil recruitment from the bone marrow of dextran sulfate sodium animals. Functional inhibition of IL-6 led to reduced systemic and pulmonary neutrophilia, but it did not attenuate established colitis pathology. These data suggest that systemic bacteremia and pyrexia drive IL-6 secretion, which is a critical driver for pulmonary manifestation of IBD. Targeting IL-6 may reduce neutrophil-associated extraintestinal manifestations in IBD patients.
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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 |
Rutting S, Xenaki D, Lau E, Horvat J, Wood LG, Hansbro PM, Oliver BG, 'Dietary omega-6, but not omega-3, polyunsaturated or saturated fatty acids increase inflammation in primary lung mesenchymal cells', American Journal of Physiology - Lung Cellular and Molecular Physiology, 314 L922-L935 (2018) [C1] Obesity is an important risk factor for developing severe asthma. Dietary fatty acids, which are increased in sera of obese individuals and after high-fat meals, activate the inna... [more] Obesity is an important risk factor for developing severe asthma. Dietary fatty acids, which are increased in sera of obese individuals and after high-fat meals, activate the innate immune system and induce inflammation. This study investigated whether dietary fatty acids directly cause inflammation and/or synergize with obesity-induced cytokines in primary human pulmonary fibroblasts in vitro. Fibroblasts were challenged with BSA-conjugated fatty acids [¿-6 polyunsaturated fatty acids (PUFAs) and ¿-3 PUFAs or saturated fatty acids (SFAs)], with or without TNF-a, and release of the proinflammatory cytokines, IL-6 and CXCL8, was measured. We found that the ¿-6 PUFA arachidonic acid (AA), but not ¿-3 PUFAs or SFAs, upregulates IL-6 and CXCL8 release. Combined AA and TNF-a challenge resulted in substantially greater cytokine release than either alone, demonstrating synergy. Synergistic upregulation of IL-6, but not CXCL8, was mainly mediated via cyclooxygenase (COX). Inhibition of p38 MAPK reduced CXCL8 release, induced by AA and TNF-a alone, but not in combination. Synergistic CXCL8 release, following AA and TNF-a challenge, was not medicated via a single signaling pathway (MEK1, JNK, phosphoinositide 3-kinase, and NF-¿B) nor by hyperactivation of NF-¿B or p38. To investigate if these findings occur in other airway cells, effects of AA in primary human airway smooth muscle (ASM) cells and human bronchial epithelial cells were also investigated. We found proinflammatory effects in ASM cells but not epithelial cells. This study suggests that diets rich in ¿-6 PUFAs might promote airway inflammation via multiple pathways, including COX-depen-dent and-independent pathways, and in an obese person, may lead to more severe airway inflammation.
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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 |
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 |
Pinkerton JW, Kim RY, Robertson AAB, Hirota JA, Wood LG, Knight DA, et al., 'Inflammasomes in the lung', Molecular Immunology, 86 44-55 (2017) [C1] Innate immune responses act as first line defences upon exposure to potentially noxious stimuli. The innate immune system has evolved numerous intracellular and extracellular rece... [more] Innate immune responses act as first line defences upon exposure to potentially noxious stimuli. The innate immune system has evolved numerous intracellular and extracellular receptors that undertake surveillance for potentially damaging particulates. Inflammasomes are intracellular innate immune multiprotein complexes that form and are activated following interaction with these stimuli. Inflammasome activation leads to the cleavage of pro-IL-1ß and release of the pro-inflammatory cytokine, IL-1ß, which initiates acute phase pro-inflammatory responses, and other responses are also involved (IL-18, pyroptosis). However, excessive activation of inflammasomes can result in chronic inflammation, which has been implicated in a range of chronic inflammatory diseases. The airways are constantly exposed to a wide variety of stimuli. Inflammasome activation and downstream responses clears these stimuli. However, excessive activation may drive the pathogenesis of chronic respiratory diseases such as severe asthma and chronic obstructive pulmonary disease. Thus, there is currently intense interest in the role of inflammasomes in chronic inflammatory lung diseases and in their potential for therapeutic targeting. Here we review the known associations between inflammasome-mediated responses and the development and exacerbation of chronic lung diseases.
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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 |
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 |
Liu G, Cooley MA, Nair PM, Donovan C, Hsu AC, Jarnicki AG, et al., 'Airway remodelling and inflammation in asthma are dependent on the extracellular matrix protein fibulin-1c', JOURNAL OF PATHOLOGY, 243 510-523 (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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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 |
Simpson JL, Baines KJ, Horvat JC, Essilfie AT, Brown AC, Tooze M, et al., 'COPD is characterized by increased detection of Haemophilus influenzae, Streptococcus pneumoniae and a deficiency of Bacillus species', Respirology, 21 697-704 (2016) [C1] Background and objective Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow limitation and inflammation. Airway bacterial colonization is increas... [more] Background and objective Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow limitation and inflammation. Airway bacterial colonization is increased in COPD; however, the role of potentially pathogenic and non-pathogenic bacteria in the pathogenesis of disease is unclear. This study characterized the presence of bacteria in a well-characterized cohort of adults with COPD and healthy controls. Methods Adults with COPD (n = 70) and healthy controls (n = 51) underwent clinical assessment and sputum induction. Sputum was dispersed, and total and differential cell counts were performed. Bacteria were cultured, identified and enumerated. Supernatants were assessed for neutrophil elastase (NE) and IL-1ß. Common respiratory pathogens were also determined using real-time PCR. Results Participants with COPD had a typical neutrophilic inflammatory profile. The total load of bacteria was increased in COPD and was associated with poorer respiratory health status, as measured by the St George's Respiratory Questionnaire (Spearman's r = 0.336, P = 0.013). Significantly lower levels of culturable Bacillus species were identified compared with healthy controls. PCR analyses revealed increased rates of detection of potentially pathogenic bacteria with Haemophilus influenzae detection associated with higher sputum levels of NE and IL-1ß, while Streptococcus pneumoniae was more common in male ex-smokers with emphysema and a deficit in diffusion capacity. Conclusion Non-pathogenic and pathogenic bacteria were altered in the sputum of patients with COPD. These observations highlight the potential to identify treatment and management strategies that both target specific bacterial pathogens and restore the microbial balance, which may lead to reductions in inflammation and subsequent improvements in lung health.
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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.
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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]
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2016 |
Gang L, Hsu A, Cooley MA, Jarnicki AG, Nair PM, Haw TJ, et al., 'Fibulin-1 regulates the pathogenesis of tissue remodeling in respiratory diseases', Journal of Clinical Investigation Insight, 1 (2016) [C1]
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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]
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2015 |
Zouikr I, Ahmed AF, Horvat JC, Beagley KW, Clifton VL, Ray A, et al., 'Programming of formalin-induced nociception by neonatal LPS exposure: Maintenance by peripheral and central neuroimmune activity', Brain, Behavior, and Immunity, 44 235-246 (2015) [C1] The immune and nociceptive systems are shaped during the neonatal period where they undergo fine-tuning and maturation. Painful experiences during this sensitive period of develop... [more] The immune and nociceptive systems are shaped during the neonatal period where they undergo fine-tuning and maturation. Painful experiences during this sensitive period of development are known to produce long-lasting effects on the immune and nociceptive responses. It is less clear, however, whether inflammatory pain responses are primed by neonatal exposure to mild immunological stimuli, such as with lipopolysaccharide (LPS). Here, we examine the impact of neonatal LPS exposure on inflammatory pain responses, peripheral and hippocampal interleukin-1ß (IL-1ß), as well as mast cell number and degranulation in preadolescent and adult rats. Wistar rats were injected with LPS (0.05 mg/kg IP, Salmonella enteritidis) or saline on postnatal days (PNDs) 3 and 5 and later subjected to the formalin test at PNDs 22 and 80-97. At both time-points, and one-hour after formalin injection, blood and hippocampus were collected for measuring circulating and central IL-1ß levels using ELISA and Western blot, respectively. Paw tissue was also isolated to assess mast cell number and degree of degranulation using Toluidine Blue staining. Behavioural analyses indicate that at PND 22, LPS-challenged rats displayed enhanced flinching (p<.01) and licking (p<.01) in response to formalin injection. At PNDs 80-97, LPS-challenged rats exhibited increased flinching (p<.05), an effect observed in males only. Furthermore, neonatal LPS exposure enhanced circulating IL-1ß and mast cell degranulation in preadolescent but not adult rats following formalin injection. Hippocampal IL-1ß levels were increased in LPS-treated adult but not preadolescent rats in response to formalin injection. These data suggest neonatal LPS exposure produces developmentally regulated changes in formalin-induced behavioural responses, peripheral and central IL-1ß levels, as well as mast cell degranulation following noxious stimulation later in life. These findings highlight the importance of immune activation during the neonatal period in shaping immune response and pain sensitivity later in life. This is of clinical relevance given the high prevalence of bacterial infection during the neonatal period, particularly in the vulnerable population of preterm infants admitted to neonatal intensive care units.
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2015 |
Sozo F, Horvat JC, Essilfie A-T, O'Reilly M, Hansbro PM, Harding R, 'Altered lung function at mid-adulthood in mice following neonatal exposure to hyperoxia.', Respir Physiol Neurobiol, 218 21-27 (2015) [C1]
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2015 |
Singanayagam A, Glanville N, Walton RP, Aniscenko J, Pearson RM, Pinkerton JW, et al., 'A short-term mouse model that reproduces the immunopathological features of rhinovirus-induced exacerbation of COPD.', Clin Sci (Lond), 129 245-258 (2015) [C1]
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2015 |
Kim RY, Pinkerton JW, Gibson PG, Cooper MA, Horvat JC, Hansbro PM, 'Inflammasomes in COPD and neutrophilic asthma', THORAX, 70 1199-1201 (2015) [C1]
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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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2014 |
O'Reilly M, Hansbro PM, Horvat JC, Beckett EL, Harding R, Sozo F, 'Bronchiolar Remodeling in Adult Mice Following Neonatal Exposure to Hyperoxia: Relation to Growth', Anatomical Record, 297 758-769 (2014) [C1] Preterm infants who receive supplemental oxygen for prolonged periods are at increased risk of impaired lung function later in life. This suggests that neonatal hyperoxia induces ... [more] Preterm infants who receive supplemental oxygen for prolonged periods are at increased risk of impaired lung function later in life. This suggests that neonatal hyperoxia induces persistent changes in small conducting airways (bronchioles). Although the effects of neonatal hyperoxia on alveolarization are well documented, little is known about its effects on developing bronchioles. We hypothesized that neonatal hyperoxia would remodel the bronchiolar walls, contributing to altered lung function in adulthood. We studied three groups of mice (C57BL/6J) to postnatal day 56 (P56; adulthood) when they either underwent lung function testing or necropsy for histological analysis of the bronchiolar wall. One group inhaled 65% O2 from birth until P7, after which they breathed room air; this group experienced growth restriction (HE+GR group). We also used a group in which hyperoxia-induced GR was prevented by dam rotation (HE group). A control group inhaled room air from birth. At P56, the bronchiolar epithelium of HE mice contained fewer Clara cells and more ciliated cells, and the bronchiolar wall contained ~25% less collagen than controls; in HE+GR mice the bronchiolar walls had ~13% more collagen than controls. Male HE and HE+GR mice had significantly thicker bronchiolar epithelium than control males and altered lung function (HE males: greater dynamic compliance; HE+GR males: lower dynamic compliance). We conclude that neonatal hyperoxia remodels the bronchiolar wall and, in adult males, affects lung function, but effects are altered by concomitant growth restriction. Our findings may partly explain the reports of poor lung function in ex-preterm children and adults. Anat Rec, 297:758-769, 2014. © 2014 Wiley Periodicals, Inc.
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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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2014 |
Goggins B, Minahan K, Kostakis A, Shalwitz R, Horvat J, Keely S, 'Stabilisation of epithelial hypoxia-inducible factor reverses colitis through accelerated restitution', FASEB JOURNAL, 28 (2014)
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2013 |
Goggins BJ, Chaney C, Radford-Smith GL, Horvat JC, Keely S, 'Hypoxia and Integrin-Mediated Epithelial Restitution during Mucosal Inflammation.', Front Immunol, 4 272 (2013) [C1]
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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 P, Beckett E, Stevens R, Jarnicki A, Wark P, Foster P, 'A short-term model of COPD identifies a role for mast cell tryptase', EUROPEAN RESPIRATORY JOURNAL, 42 (2013) [C3]
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2013 |
Fung KY, Mangan NE, Cumming H, Horvat JC, Mayall JR, Stifter SA, et al., 'Interferon-epsilon Protects the Female Reproductive Tract from Viral and Bacterial Infection', SCIENCE, 339 1088-1092 (2013) [C1]
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2013 |
Beckett EL, Stevens RL, Jarnicki AG, Kim RY, Hanish I, Hansbro NG, et al., 'A new short-term mouse model of chronic obstructive pulmonary disease identifies a role for mast cell tryptase in pathogenesis', The Journal of Allergy and Clinical Immunology, 131 752-762 (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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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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2012 |
Wynne OL, Horvat JC, Smith R, Hansbro PM, Clifton VL, Hodgson DM, 'Effect of neonatal respiratory infection on adult BALB/c hippocampal glucocorticoid and mineralocorticoid receptors', Developmental Psychobiology, 54 568-575 (2012) [C1]
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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]
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2011 |
Essilfie A-T, Simpson JL, Horvat JC, Preston JA, Dunkley ML, Foster PS, et al., 'Haemophilus influenzae infection drives IL-17-mediated neutrophilic allergic airways disease', PLoS Pathogens, 7 e1002244 (2011) [C1]
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2011 |
Asquith KL, Horvat JC, Kaiko GE, Carey AJ, Beagley KW, Hansbro PM, Foster PS, 'Interleukin-13 promotes susceptibility to chlamydial infection of the respiratory and genital tracts', PLoS Pathogens, 7 (2011) [C1]
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2011 |
Wynne OL, Horvat JC, Kim RY, Ong LK, Smith R, Hansbro PM, et al., 'Neonatal respiratory infection and adult re-infection: Effect on glucocorticoid and mineralocorticoid receptors in the hippocampus in BALB/c mice', Brain Behavior and Immunity, 25 1214-1222 (2011) [C1]
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2011 |
Wynne OL, Horvat JC, Osei-Kumah A, Smith R, Hansbro PM, Clifton VL, Hodgson DM, 'Early life infection alters adult BALB/c hippocampal gene expression in a sex specific manner', Stress-the International Journal on the Biology of Stress, 14 247-261 (2011) [C1]
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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]
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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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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]
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2010 |
Starkey MR, Horvat JC, Kim RY, Hansbro PM, 'Reply', Journal of Allergy and Clinical Immunology, 125 1415 (2010) [C3]
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2008 |
Kaiko GE, Horvat JC, Beagley KW, Hansbro PM, 'Immunological decision-making: How does the immune system decide to mount a helper T-cell response?', Immunology, 123 326-338 (2008) [C1]
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2008 |
Hansbro NG, Horvat JC, Wark PA, Hansbro PM, 'Understanding the mechanisms of viral induced asthma: New therapeutic directions', Pharmacology & Therapeutics, 117 313-353 (2008) [C1]
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2007 |
Horvat JC, Beagley KW, Wade MA, Preston JA, Hansbro NG, Hickey DK, et al., 'Neonatal chlamydial infection induces mixed T-cell responses that drive allergic airway disease', American Journal of Respiratory and Critical Care Medicine, 176 556-564 (2007) [C1]
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2007 |
Preston JA, Essilfie AT, Horvat JC, Wade MA, Beagley KW, Gibson PG, et al., 'Inhibition of allergic airways disease by immunomodulatory therapy with whole killed Streptococcus pneumoniae', Vaccine, 25 8154-8162 (2007) [C1]
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2006 |
Skelding KA, Hickey DK, Horvat JC, Bao SS, Roberts KG, Read JM, et al., 'Comparison of intranasal and transcutaneous immunization for induction of protective immunity against Chlamydia muridarum respiratory tract infection', Vaccine, 24 355-366 (2006) [C1]
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2004 |
Hansbro PM, Beagley KW, Horvat JC, Gibson PG, 'Role of atypical bacterial infection of the lung in predisposition/protection of asthma', Pharmacology and Therapeutics, 101 193-210 (2004) [C1]
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Review (1 outputs)
Year | Citation | Altmetrics | Link | ||||||||
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2015 |
Mateer SW, Maltby S, Marks E, Foster PS, Horvat JC, Hansbro PM, Keely S, 'Potential mechanisms regulating pulmonary pathology in inflammatory bowel disease.', J Leukoc Biol (2015) [C1]
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Conference (163 outputs)
Year | Citation | Altmetrics | Link | ||||||||
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2023 |
Barnes J, Plank M, Asquith K, Maltby S, Rodrigues SL, Kaiko G, et al., 'T-helper-22 cells develop independently of Th17 cells during bacterial infection', RESPIROLOGY (2023)
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2023 |
Williams EJ, Smith B, Pillar AL, Daly K, Mayall JR, Horvat JC, Wood LG, 'Ferrous iron (Fe2+) increases pro-inflammatory cytokine production of peripheral blood mononuclear cells in response to influenza A virus (IAV)', PROCEEDINGS OF THE NUTRITION SOCIETY (2023)
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2023 |
Mayall J, Pillar A, Daly K, Brown A, Essilfie A-T, Gomez H, et al., 'LSC-2023-Iron metabolism determines the outcome of influenza A virus infection', EUROPEAN RESPIRATORY JOURNAL, IA, Milan (2023)
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2021 |
Goggins BJ, Minahan K, Sherwin S, Soh WS, Pryor J, Bruce JK, et al., 'PHARMACOLOGICAL HIF-1 STABILIZATION PROMOTES INTESTINAL EPITHELIAL HEALING THROUGH REGULATION OF a-INTEGRIN EXPRESSION AND FUNCTION', GASTROENTEROLOGY, ELECTR NETWORK (2021)
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2020 |
Lyall D, Hansbro P, Horvat J, Stanwell P, 'Quantitative Nondestructive Assessment of Paenibacillus larvae in Apis mellifera Hives', Advances in Intelligent Systems and Computing, Universität der Bundeswehr München, Munich, Germany (2020) [E1]
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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 |
Mateer S, Marks E, Maltby S, Goggins B, Horvat J, Hansbro P, Keely S, 'Pulmonary retention of PMN attracts primed intestinal lymphocytes in a mouse model of inflammatory bowel disease', FASEB JOURNAL (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 |
Goggins B, Minahan K, Marks E, Mateer S, Cardona J, Knight D, et al., 'Hypoxia inducible factor (HIF)-1 accelerates epithelial wound healing through integrin regulation', JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY (2014) [E3]
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2014 |
Cardona J, Marks E, Goggins B, Mateer S, Minahan K, Horvat J, Keely S, 'The role of antibiotics in the development of food allergy', JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY (2014) [E3]
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2014 |
Mateer S, Maltby S, Marks E, Goggins B, Horvat J, Hansbro P, Keely S, 'Immune cell mis-homing drives secondary organ inflammation in inflammatory bowel disease; a focus on the respiratory system', JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY (2014) [E3]
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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]
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Nova | |||||||||
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)
|
||||||||||
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)
|
||||||||||
2013 |
Hansbro P, Beckett E, Stevens R, Jarnicki A, Kim R, Hanish I, et al., 'A short-term model of COPD identifies a role for mast cell tryptase', JOURNAL OF IMMUNOLOGY, Honolulu, HI (2013) [E3]
|
||||||||||
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]
|
||||||||||
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]
|
||||||||||
2012 |
Stifter SA, Fung K, Horvat JC, Hansbro PM, De Weerd NA, Hertzog PJ, 'Expression, purification and biological characterisation of a novel type I interferon, IFN epsilon', Immunology, Glasgow, Scotland (2012) [E3]
|
||||||||||
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]
|
||||||||||
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]
|
||||||||||
2011 |
O'Reilly M, Hansbro PM, Horvat JC, Sozo F, Harding R, 'Inhalation of hyperoxic gas in the neonatal period has long-term effects on the pulmonary airways', Journal of Developmental Origins of Health and Disease, Portland, Oregon (2011) [E3]
|
||||||||||
2011 |
Wynnea O, Horvat JC, Kim RY, Ong LK, Smith R, Hansbro PM, et al., 'Sex differences in the effect of neonatal infection and adult re-infection on hippocampal corticosterone receptors and stress response outcomes', Brain, Behavior, and Immunity, Chicago, Illinois (2011) [E3]
|
||||||||||
2011 |
Hansbro PM, Horvat JC, Essilfie A-T, Kim RY, Simpson JL, Dunkley ML, et al., 'Infection-induced neutrophilic allergic airways disease is resistant to steroid treatment', American Journal of Respiratory and Critical Care Medicine, Denver, CO (2011) [E3]
|
||||||||||
2011 |
Horvat JC, Essilfie A-T, Kim RY, Simpson JL, Dunkley ML, Beagley KW, et al., 'Investigation of infection-induced steroid resistant asthma', Respirology, Perth, WA (2011) [E3]
|
||||||||||
2010 |
Hansbro PM, Essilfie A-T, Simpson JL, Dunkley ML, Horvat JC, Gibson PG, Foster PS, 'Haemophilus influenzae induces IL-17-mediated neutrophilic allergic airways disease', American Journal of Respiratory and Critical Care Medicine, New Orleans (2010) [E3]
|
||||||||||
2010 |
O'Reilly M, Harding R, Beckett EL, Horvat JC, Hansbro PM, Sozo F, 'Exposure of the immature mouse lung to hyperoxic gas: do structural changes in the lung cause long-term changes in lung function?', 24th Fetal and Neonatal Physiology Workshop of Australia and New Zealand. Program and Abstracts, Wellington, NZ (2010) [E3]
|
||||||||||
2010 |
Fung K, Cumming H, Mangan N, Horvat JC, Hansbro PM, Hertzog P, 'Interferon epsilon regulates reproductive tract immunity to Chlamydia infection', Journal of Reproductive Immunology, Palm Cove, QLD (2010) [E3]
|
||||||||||
2009 |
Fung KY, Cumming H, Mangan N, Stifter S, Horvat JC, Hansbro PM, Hertzog PJ, 'Characterisation of a novel, constitutive cytokine that regulates mucosal immunity in the reproductive tract', Cytokine, Lisbon, Portugal (2009) [E3]
|
||||||||||
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]
|
||||||||||
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]
|
||||||||||
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]
|
||||||||||
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]
|
||||||||||
2008 |
Wynne OL, Horvat JC, Smith R, Hansbro PM, Clifton VL, Hodgson DM, 'Impact of neonatal infection on adult hippocampal glucocorticoid receptor, mineralocorticoid receptor and corticotrophin releasing hormone mRNA abundance', Proceedings of the Australian Neuroscience Society, Hobart, TAS (2008) [E3]
|
||||||||||
2008 |
Hansbro PM, Horvat JC, Beagley KW, Gibson PG, Foster PS, 'Neutrophil influx during chlamydial lung infection determines the phenotype of allergic airways disease', American Journal of Respiratory and Critical Care Medicine, Toronto, ONT (2008) [E3]
|
||||||||||
2008 |
Horvat JC, Beagley KW, Gibson PG, Foster PS, Hansbro PM, 'Neutrophil influx during chlamydial lung infection determines the phenotype of allergic airways disease', Respirology, Melbourne, VIC (2008) [E3]
|
||||||||||
2008 |
Essilfie A-T, Preston JA, Horvat JC, Dunkley ML, Foster PS, Gibson PG, et al., 'Haemophilus influenzae (Hi) infection in asthma may drive the development of neutrophilic asthma (NA)', Respirology, Melbourne, VIC (2008) [E3]
|
||||||||||
2008 |
Wynne OL, Horvat JC, Smith R, Hansbro PM, Clifton VL, Hodgson DM, 'Impact of neonatal infection on adult hippocampal glucocorticoid receptor and mineralocorticoid receptor abundance', 15th Annual Meeting of the Psychoneuroimmunology Research Society: Program, Madison, WISC (2008) [E3]
|
||||||||||
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]
|
||||||||||
2007 |
Horvat JC, Preston JA, Gibson PG, Beagley KW, Foster PS, Hansbro PM, 'Development of allergic airways disease (AAD) is differentially affected by the timing of chlamydial infection relative to allergic sensitization', American Journal of Respiratory and Critical Care Medicine, San Francisco, Calif. (2007) [E3]
|
||||||||||
2007 |
Horvat JC, Garside CG, Wade MA, Preston JA, Hansbro NG, Gibson PG, et al., 'Development of allergic airways disease is differentially affected by chlamydial respiratory infection at different ages', American Journal of Respiratory and Critical Care Medicine, San Francisco, Calif. (2007) [E3]
|
||||||||||
2007 |
Wynne OL, Horvat JC, Smith R, Hansbro PM, Clifton VL, Hodgson DM, 'Impact of neonatal infection on adult hippocampal corticosterone receptor abundance and circulating corticosterone', Early Human Development, Perth (2007) [E3]
|
||||||||||
2007 |
Wynne OL, Horvat JC, Hansbro PM, Clifton VL, Hodgson DM, 'Impact of postnatal stress on neuroendocrine development and function in adulthood in the mouse', Fetal & Neonatal Workshop of Australia and New Zealand 21st Annual Meeting. Abstracts, Melbourne, VIC (2007) [E3]
|
||||||||||
2007 |
Essiflie A, Preston JA, Horvat JC, Dunkley ML, Foster PS, Gibson PG, et al., 'Elucidating the association between Haemophilus influenzae infection and neutrophilic allergic airways disease using mouse models', Immuno 2007: 13th International Congress of Immunology. Abstracts and Posters, Rio de Janeiro, Brazil (2007) [E3]
|
||||||||||
2007 |
Horvat JC, Moller CG, Wade MA, Preston JA, Hansbro NG, Gibson PG, et al., 'Allergic airways disease (AAD) is differentially affected by chlamydial lung infection at different stages of life', Respirology (TSANZ Abstracts-Posters), Auckland (2007) [E3]
|
||||||||||
2007 |
Horvat JC, Preston JA, Gibson PG, Beagley KW, Foster PS, Hansbro PM, 'Timing of chlamydial infection relative to allergen exposure differentially affects allergic airways disease', Respirology (TSANZ Abstracts-Posters), Auckland (2007) [E3]
|
||||||||||
2006 |
Horvat JC, Preston JA, Gibson PG, Beagley KW, Foster PS, Hansbro PM, 'Exacerbation of Allergic Airways Disease (AAD) by Chlamydia is Differentially Affected by the Timing of Infection Relative to Allergen Exposure', Immunology and Cell Biology, Auckland, NZ (2006) [E3]
|
||||||||||
2006 |
Preston JA, Horvat JC, Beagley KW, Foster PS, Gibson PG, Hansbro PM, 'Streptococcus pneumoniae (SPN) lung infection suppresses hallmark features of a mouse model of asthma', Immunology and Cell Biology, Auckland, NZ (2006) [E3]
|
||||||||||
2006 |
Horvat JC, Moller CG, Wade MA, Preston JA, Hansbro NG, Gibson PG, et al., 'The development of allergic airways disease (AAD) is differently affected by chlamydial lung infection at different stages of life', Immunology and Cell Biology, Auckland, NZ (2006) [E3]
|
||||||||||
2006 |
Horvat JC, Wade MA, Preston JA, Hansbro NG, Gibson PG, Beagley KW, et al., 'Early life chlamydial lung infection enhances allergic airways disease (AAD)', Respirology, Canberra (2006) [E3]
|
||||||||||
2006 |
Preston JA, Horvat JC, Wade MA, Beagley KW, Foster PS, Gibson PG, Hansbro PM, 'Inhibition of allergic lung disease by respiratory streptococcus pneumoniae infection', Respirology, Canberra (2006) [E3]
|
||||||||||
2006 |
Horvat JC, Wade MA, Preston JA, Hansbro NG, Gibson PG, Beagley KW, et al., 'Neonatal chlamydial infection exacerbates allergic airways disease', Abstracts ATS 2006 International Conference, San Diego, California (2006) [E3]
|
||||||||||
2006 |
Preston JA, Horvat JC, Beagley KW, Foster PS, Gibson PG, Hansbro PM, 'Respiratory Streptococcus pneumoniae infection decreases key inflammatory responses in a mouse model of asthma', Abstracts ATS 2006 International Conference, San Diego, California (2006) [E3]
|
||||||||||
2006 |
Preston JA, Horvat JC, Wade MA, Beagley KW, Foster PS, Gibson PG, Hansbro PM, 'Inhibition of allergic lung disease by respiratory Streptococcus pneumoniae infection', 5th International Symposium on Pneumococci and Pneumococcal Diseases, Alice Springs (2006) [E3]
|
||||||||||
2006 |
Preston JA, Horvat JC, Wade MA, Beagley KW, Foster PS, Gibson PG, Hansbro PM, 'The influence of allergic airways disease on the immune response to respiratory Streptococcus pneumoniae infection', 5th International Symposium on Pneumococci and Pneumococcal Diseases, Alice Springs (2006) [E3]
|
||||||||||
2005 |
Horvat JC, Wade MA, Preston JA, Newcombe N, Ferguson AL, Kaiko G, et al., 'Neonatal But Not Adult Chlamydial Infection Induces the Development of Allergic Airways Disease Through Novel Mechanisms Involving Inflammation of Mixed Phenotype', Tissue Antigens, Melbourne, Australia (2005) [E3]
|
||||||||||
2005 |
Horvat JC, Preston JA, Hansbro NG, Ferguson AL, Gibson PG, Beagley KW, et al., 'Neonatal chlamydial infection inhibits the development of allergic airway inflammation in adult mice', Inflammation Research, Melbourne, Australia (2005) [E3]
|
||||||||||
2005 |
Preston JA, Horvat JC, Beagley KW, Foster PS, Gibson PG, Hansbro PM, 'Timing of Streptococcus Pneumoniae (pnc) infection determines the magnitute of the effect on allergic airways inflammation (AAI) in a mouse model of asthma', Respirology, Perth Convention Exhibition Centre (2005) [E3]
|
||||||||||
2005 |
Preston JA, Horvat JC, Beagley KW, Foster PS, Gibson PG, Hansbro PM, 'Respiratory Streptococcus Pneumoniae Infection Decreases Eosinophilia and Mucus Cell Hyperplasia in a Mouse Model of Asthma', Respirology, Perth Convention Exhibition Centre (2005) [E3]
|
||||||||||
2005 |
Skelding KA, Hickey DK, Horvat JC, Hansbro PM, Bao S, Beagley KW, 'Combined transcutaneous and intranasal immunisation protects against genital tract Chlamydial infection', Proceedings of the Twelfth International Congress of Mucosal Immunology, Boston, Massachusetts, USA. (2005) [E3]
|
||||||||||
2005 |
Skelding KA, Hickey DK, Horvat JC, Hansbro PM, Bao S, Beagley KW, 'Comparison of intranasal and transcutaneous immunisation for the protection against Chlamydial pneumonia', Proceedings of the Twelfth International Congress of Mucosal Immunology, Boston, Massachusetts (2005) [E3]
|
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Show 160 more conferences |
Preprint (5 outputs)
Year | Citation | Altmetrics | Link | |||||
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2023 |
Hedley KE, Cuskelly A, Callister RJ, Horvat JC, Hodgson DM, Tadros MA, 'Autonomic Regions of the Brainstem Show a Sex-Specific Inflammatory Response to Systemic Neonatal Lipopolysaccharide (2023)
|
|||||||
2022 |
Chen L, Hoefel GA, Pathinayake PS, Reid A, Kelly C, HuiYing T, et al., 'Single cell RNA-seq identifies inflammation-induced loss of CFTR-expressing airway ionocytes in non-eosinophilic asthma (2022)
|
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2021 |
Burns G, Bruce J, Minahan K, Mathe A, Fairlie T, Cameron R, et al., 'Distinct Adaptive Immunophenotypes in duodenal mucosa but not in peripheral blood of patients with functional dyspepsia (2021)
|
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Show 2 more preprints |
Grants and Funding
Summary
Number of grants | 60 |
---|---|
Total funding | $11,331,474 |
Click on a grant title below to expand the full details for that specific grant.
20242 grants / $1,349,359
Manipulating iron metabolism in the airway mucosa for the treatment of severe asthma and COPD$1,299,359
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Professor Jay Horvat, Doctor Alexandra Brown, Ama Essilfie, Dr Ama-Tawiah Essilfie, Associate Professor David Reid, Professor Jodie Simpson |
Scheme | Ideas Grants |
Role | Lead |
Funding Start | 2024 |
Funding Finish | 2026 |
GNo | G2300370 |
Type Of Funding | C1100 - Aust Competitive - NHMRC |
Category | 1100 |
UON | Y |
Newcastle Human Organoid Program for Effective New Therapies (New HOPE – New Therapies) $50,000
Funding body: Jessie Speight Bequest
Funding body | Jessie Speight Bequest |
---|---|
Project Team | Professor Jay Horvat, Professor Chris Dayas, Conjoint Associate Professor Christopher Grainge, Doctor Gerard Kaiko, Professor Simon Keely |
Scheme | Research Funding |
Role | Lead |
Funding Start | 2024 |
Funding Finish | 2024 |
GNo | G2400300 |
Type Of Funding | Scheme excluded from IGS |
Category | EXCL |
UON | Y |
20234 grants / $1,751,714
Personalising the management of obesity-associated asthma using medical nutrition therapy and physical activity prescription: The IDEAL Study$1,501,947
Funding body: Department of Health and Aged Care
Funding body | Department of Health and Aged Care |
---|---|
Project Team | Doctor Hayley Scott, Professor Lisa Wood, Doctor Sarah Valkenborghs, Professor Anne Dixon, Professor Jay Horvat, Doctor Natasha Weaver, Dr Serene Yoong, Doctor Bronwyn Berthon, Doctor Evan Williams, Doctor Alexandra Brown, Dr Sze Yoong |
Scheme | MRFF - PPHRI - Chronic Respiratory Conditions |
Role | Investigator |
Funding Start | 2023 |
Funding Finish | 2024 |
GNo | G2200660 |
Type Of Funding | C1300 - Aust Competitive - Medical Research Future Fund |
Category | 1300 |
UON | Y |
Targeting IL-1 family cytokines as a unified approach to treat asthma exacerbations$205,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Doctor Pedro Garcia Sobrinho, Professor Jay Horvat, Un-named Student, Professor Paul Foster |
Scheme | Postgraduate Research Scholarship |
Role | Lead |
Funding Start | 2023 |
Funding Finish | 2026 |
GNo | G2300067 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
Investigating the role of iron status and supplementation during pregnancy on respiratory disease in children$30,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Doctor Henry Gomez, Associate Professor Adam Collison, Professor Jay Horvat, Professor Craig Pennell |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2023 |
Funding Finish | 2023 |
GNo | G2300103 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
Investigating how excess nutrients in obesity affect immune responses to respiratory virus infection$14,767
Funding body: Hunter New England Local Health District
Funding body | Hunter New England Local Health District |
---|---|
Project Team | Doctor Lily Williams, Doctor Alexandra Brown, Doctor Alexandra Brown, Professor Jay Horvat, Doctor Evan Williams, Doctor Geoffrey Tyler |
Scheme | John Hunter Hospital Charitable Trust Grant |
Role | Investigator |
Funding Start | 2023 |
Funding Finish | 2023 |
GNo | G2300690 |
Type Of Funding | C2400 – Aust StateTerritoryLocal – Other |
Category | 2400 |
UON | Y |
20225 grants / $716,464
Implementation of lung function analyses that may facilitate earlier detection of harmful dust exposure and occupational lung disease$513,691
Funding body: Coal Services Health and Safety Trust
Funding body | Coal Services Health and Safety Trust |
---|---|
Project Team | Professor Jay Horvat, Doctor Dusan Ilic, Doctor Jemma Mayall, Professor Carole James, Conjoint Professor Peter Wark, Associate Professor Alexander Donald, Associate Professor Deborah Yates, A/Prof Brian Oliver, Dr Katrina Tonga, Dr David Meredith |
Scheme | Research Project |
Role | Lead |
Funding Start | 2022 |
Funding Finish | 2025 |
GNo | G2100436 |
Type Of Funding | C3200 – Aust Not-for Profit |
Category | 3200 |
UON | Y |
Development of an accurate biological test for the monitoring and assessment of occupational dust inhalation in high dust industries$106,000
Funding body: The University of Newcastle Research Associates Ltd (TUNRA)
Funding body | The University of Newcastle Research Associates Ltd (TUNRA) |
---|---|
Project Team | Professor Jay Horvat, Professor Andrew Fleming, Doctor Dusan Ilic, Mr Prabhasha Jayasundara, Doctor Jemma Mayall |
Scheme | Scholarships |
Role | Lead |
Funding Start | 2022 |
Funding Finish | 2025 |
GNo | G2101352 |
Type Of Funding | Scheme excluded from IGS |
Category | EXCL |
UON | Y |
Investigating the cardiopulmonary impacts of prolonged exposure to bushfire smoke particulate matter and other environmental hazards in Regional Australia$75,000
Funding body: National Heart Foundation of Australia
Funding body | National Heart Foundation of Australia |
---|---|
Project Team | Doctor Tatt Jhong Haw, Doctor Henry Gomez, Professor Jay Horvat, Professor Doan Ngo |
Scheme | Vanguard Grant |
Role | Investigator |
Funding Start | 2022 |
Funding Finish | 2022 |
GNo | G2100499 |
Type Of Funding | C1700 - Aust Competitive - Other |
Category | 1700 |
UON | Y |
Treatment with a hepcidin mimetic to regulate iron levels in respiratory diseases such as asthma, COPD$11,289
Funding body: Protagonist Therapeutics Inc
Funding body | Protagonist Therapeutics Inc |
---|---|
Project Team | Professor Jay Horvat, Doctor Alexandra Brown |
Scheme | Research Grant |
Role | Lead |
Funding Start | 2022 |
Funding Finish | 2022 |
GNo | G2200942 |
Type Of Funding | C3400 – International For Profit |
Category | 3400 |
UON | Y |
Targeting the NLRP3 inflammsome to improve the immune response of obese individuals to Influenza A virus$10,484
Funding body: Hunter New England Local Health District
Funding body | Hunter New England Local Health District |
---|---|
Project Team | Doctor Evan Williams, Doctor David Arnold, Doctor Bronwyn Berthon, Professor Jay Horvat, Doctor Lily Williams |
Scheme | John Hunter Hospital Charitable Trust Grant |
Role | Investigator |
Funding Start | 2022 |
Funding Finish | 2022 |
GNo | G2200188 |
Type Of Funding | C2400 – Aust StateTerritoryLocal – Other |
Category | 2400 |
UON | Y |
20216 grants / $978,029
ER stress-Unfolded Protein Response a critical metabolic pathway for airway remodelling in asthma$811,596
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Conjoint Professor Peter Wark, Professor Jay Horvat, Doctor Prabuddha Pathinayake, Professor Philip Hansbro, A/Prof Brian Oliver, Doctor Alan Hsu, Doctor Alexandra Brown, Doctor Gerard Kaiko, Doctor Katie Baines |
Scheme | Ideas Grants |
Role | Investigator |
Funding Start | 2021 |
Funding Finish | 2023 |
GNo | G2000560 |
Type Of Funding | C1100 - Aust Competitive - NHMRC |
Category | 1100 |
UON | Y |
Neoantigen immunopeptidomics for the development of immunotherapies for the treatment of diffuse intrinsic pontine glioma (DIPG) $108,251
Funding body: RUN DIPG
Funding body | RUN DIPG |
---|---|
Project Team | Professor Matt Dun, Professor Jay Horvat, Associate Professor Martin Larsen, Associate Professor Luke Hesson, Associate Professor Mark Cowley |
Scheme | Scholarship |
Role | Investigator |
Funding Start | 2021 |
Funding Finish | 2024 |
GNo | G2001148 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
Effect of obesity, hormones and hormone manipulation on metabolism in immune cells$25,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Professor Lisa Wood, Professor Jay Horvat |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2021 |
Funding Finish | 2021 |
GNo | G2001482 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
Investigating the role of sex hormones in obesity associated susceptibility to respiratory viral disease$18,182
Funding body: Hunter New England Local Health District
Funding body | Hunter New England Local Health District |
---|---|
Project Team | Doctor Evan Williams, Doctor Alexandra Brown, Professor Jay Horvat, Doctor Bronwyn Berthon, Doctor David Arnold |
Scheme | John Hunter Hospital Charitable Trust Grant |
Role | Investigator |
Funding Start | 2021 |
Funding Finish | 2021 |
GNo | G2100212 |
Type Of Funding | C2400 – Aust StateTerritoryLocal – Other |
Category | 2400 |
UON | Y |
MRFF Support Grant: accelerated silicosis$10,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Professor Jay Horvat, Doctor Dusan Ilic, Professor Carole James, Conjoint Professor Peter Wark, Professor Paul Foster, Doctor Gerard Kaiko, Doctor Hock Tay, Prof Darryl Knight, A/Prof Brian Oliver, Dr Cecilia Prele |
Scheme | Research Grant |
Role | Lead |
Funding Start | 2021 |
Funding Finish | 2021 |
GNo | G2001499 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
Investigating the therapeutic potential of targeting iron in IPF$5,000
Funding body: Lung Foundation Australia
Funding body | Lung Foundation Australia |
---|---|
Project Team | Doctor Alexandra Brown, Professor Jay Horvat |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2021 |
Funding Finish | 2021 |
GNo | G2100949 |
Type Of Funding | C3200 – Aust Not-for Profit |
Category | 3200 |
UON | Y |
20204 grants / $1,433,493
Bushfire Impact on Vulnerable Groups: the respiratory burden and effective community solution$869,482
Funding body: Department of Health and Aged Care
Funding body | Department of Health and Aged Care |
---|---|
Project Team | Conjoint Professor Peter Gibson, Doctor Megan Jensen, Professor Vanessa McDonald, Professor Jay Horvat, Associate Professor Vanessa Murphy, Professor Liz Holliday, Conjoint Associate Professor Anne Vertigan |
Scheme | MRFF - EPCDR - Bushfire Impact |
Role | Investigator |
Funding Start | 2020 |
Funding Finish | 2023 |
GNo | G2000105 |
Type Of Funding | C1300 - Aust Competitive - Medical Research Future Fund |
Category | 1300 |
UON | Y |
Development of a novel effective therapy for asthma and COPD$541,849
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Professor Jay Horvat, Conjoint Professor Peter Wark, Professor Philip Hansbro |
Scheme | Development Grants |
Role | Lead |
Funding Start | 2020 |
Funding Finish | 2022 |
GNo | G1901549 |
Type Of Funding | C1100 - Aust Competitive - NHMRC |
Category | 1100 |
UON | Y |
Investigating the role of sex hormones in in obese and non-obese asthmatic females$12,162
Funding body: John Hunter Hospital Charitable Trust
Funding body | John Hunter Hospital Charitable Trust |
---|---|
Project Team | Doctor Evan Williams, Doctor Alexandra Brown, Professor Lisa Wood, Professor Jay Horvat, Doctor David Arnold, Doctor Bronwyn Berthon |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2020 |
Funding Finish | 2020 |
GNo | G2000392 |
Type Of Funding | C3200 – Aust Not-for Profit |
Category | 3200 |
UON | Y |
Investigating the health effects of bushfire smoke exposure, specifically on people with asthma, including pregnant women with asthma, and their children$10,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Conjoint Professor Peter Gibson, Associate Professor Vanessa Murphy, Professor Vanessa McDonald, Associate Professor Adam Collison, Conjoint Associate Professor Anne Vertigan, Doctor Megan Jensen, Doctor Dennis Thomas, Professor Jay Horvat, Professor Maralyn Foureur, Professor Leigh Kinsman, Professor Liz Holliday, Doctor Erin Harvey, Ms Alycia Jacob, Professor Joerg Mattes, Graeme Zosky, Wilfried Karmaus, Michele Goldman, Dr Craig Dalton |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2020 |
Funding Finish | 2020 |
GNo | G2000414 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
20194 grants / $362,742
Elucidating the roles and mechanisms of activation of NLRP3 inflammasomes and developing therapeutic interventions for severe steroid-resistant asthma$233,588
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Conjoint Professor Peter Gibson, Conjoint Professor Peter Wark, Professor Jay Horvat, Associate Professor Aeron Hurt, Professor Philip Hansbro |
Scheme | Project Grant |
Role | Investigator |
Funding Start | 2019 |
Funding Finish | 2020 |
GNo | G1900827 |
Type Of Funding | C1100 - Aust Competitive - NHMRC |
Category | 1100 |
UON | Y |
Independent study on silicosis technologies$49,577
Funding body: Humanomics Pty Ltd
Funding body | Humanomics Pty Ltd |
---|---|
Project Team | Professor Carole James, Professor Jay Horvat, Doctor Jemma Mayall, Mr John Tessier |
Scheme | Entrepreneurs' Programme: Innovation Connections |
Role | Investigator |
Funding Start | 2019 |
Funding Finish | 2021 |
GNo | G1901552 |
Type Of Funding | C3100 – Aust For Profit |
Category | 3100 |
UON | Y |
Independent study on silicosis technologies$49,577
Funding body: Department of Industry, Innovation and Science
Funding body | Department of Industry, Innovation and Science |
---|---|
Project Team | Professor Carole James, Mr John Tessier, Professor Jay Horvat, Doctor Jemma Mayall |
Scheme | Entrepreneurs' Programme: Innovation Connections |
Role | Investigator |
Funding Start | 2019 |
Funding Finish | 2021 |
GNo | G1901613 |
Type Of Funding | C1700 - Aust Competitive - Other |
Category | 1700 |
UON | Y |
Targeting cellular senescence as a novel therapeutic in Chronic Obstructive Pulmonary Disease$30,000
Funding body: Thoracic Society of Australia and New Zealand
Funding body | Thoracic Society of Australia and New Zealand |
---|---|
Project Team | Doctor Tatt Jhong Haw, Professor Philip Hansbro, Professor Jay Horvat |
Scheme | TSANZ Boehringer Ingelheim COPD Research Award |
Role | Investigator |
Funding Start | 2019 |
Funding Finish | 2019 |
GNo | G1900722 |
Type Of Funding | C3200 – Aust Not-for Profit |
Category | 3200 |
UON | Y |
20184 grants / $633,080
Defining the roles and targeting interferon-epsilon as a new therapy for influenza in asthma and COPD$363,853
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Conjoint Professor Peter Wark, Professor Jay Horvat, Professor Philip Hansbro, Associate Professor Aeron Hurt, Professor Phil Hansbro |
Scheme | Project Grant |
Role | Investigator |
Funding Start | 2018 |
Funding Finish | 2021 |
GNo | G1900905 |
Type Of Funding | C1100 - Aust Competitive - NHMRC |
Category | 1100 |
UON | Y |
Defining the roles and targeting interferon-epsilon as a new therapy for influenza in asthma and COPD$199,227
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Professor Phil Hansbro, Conjoint Professor Peter Wark, Professor Jay Horvat, Associate Professor Aeron Hurt |
Scheme | Project Grant |
Role | Investigator |
Funding Start | 2018 |
Funding Finish | 2021 |
GNo | G1700046 |
Type Of Funding | Aust Competitive - Commonwealth |
Category | 1CS |
UON | Y |
Testing treatments for asthma$50,000
Funding body: Inflazome Limited
Funding body | Inflazome Limited |
---|---|
Project Team | Professor Phil Hansbro, Professor Jay Horvat |
Scheme | Research Project |
Role | Investigator |
Funding Start | 2018 |
Funding Finish | 2018 |
GNo | G1801017 |
Type Of Funding | C3400 – International For Profit |
Category | 3400 |
UON | Y |
Investigating the Genetics of the Development of Lung Cancer$20,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Miss Vrushali Chimankar, Professor Jay Horvat, Doctor Chantal Donovan, Professor Philip Hansbro |
Scheme | Emlyn and Jennie Thomas Postgraduate Medical Research Scholarship |
Role | Lead |
Funding Start | 2018 |
Funding Finish | 2019 |
GNo | G1800717 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
20175 grants / $403,412
Characterising the epidemiological and biological effects of particulate matter exposures in coal mining to protect and improve the health of workers$171,062
Funding body: Coal Services Health and Safety Trust
Funding body | Coal Services Health and Safety Trust |
---|---|
Project Team | Professor Phil Hansbro, Professor Jay Horvat, Professor Kenneth Williams, Doctor Dusan Ilic, Professor Carole James |
Scheme | Research Project |
Role | Investigator |
Funding Start | 2017 |
Funding Finish | 2019 |
GNo | G1700782 |
Type Of Funding | C3200 – Aust Not-for Profit |
Category | 3200 |
UON | Y |
Asthma treatments$120,000
Funding body: AstraZeneca
Funding body | AstraZeneca |
---|---|
Project Team | Professor Phil Hansbro, Doctor Nicole Hansbro, Professor Jay Horvat |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2017 |
Funding Finish | 2017 |
GNo | G1700098 |
Type Of Funding | C3400 – International For Profit |
Category | 3400 |
UON | Y |
Australian Cystic Fibrosis Research Trust 2017 Innovation Grant$80,000
Funding body: Thoracic Society of Australia and New Zealand
Funding body | Thoracic Society of Australia and New Zealand |
---|---|
Project Team | Professor Jay Horvat, Professor Phil Hansbro, Conjoint Professor Peter Wark |
Scheme | Australian Cystic Fibrosis Trust Innovation Grant |
Role | Lead |
Funding Start | 2017 |
Funding Finish | 2017 |
GNo | G1700984 |
Type Of Funding | C3200 – Aust Not-for Profit |
Category | 3200 |
UON | Y |
Investigation of the role of Slc26a4 in the induction of respiratory acidosis and severe, steroid-resistant asthma$22,350
Funding body: Rebecca L Cooper Medical Research Foundation Ltd
Funding body | Rebecca L Cooper Medical Research Foundation Ltd |
---|---|
Project Team | Doctor Richard Kim, Professor Jay Horvat |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2017 |
Funding Finish | 2017 |
GNo | G1601139 |
Type Of Funding | C3200 – Aust Not-for Profit |
Category | 3200 |
UON | Y |
Flexivent FX base unit controller and software$10,000
Funding body: NSW Ministry of Health
Funding body | NSW Ministry of Health |
---|---|
Project Team | Professor Jay Horvat, Doctor Chantal Donovan, Doctor Richard Kim, Doctor Shakti Shukla, Doctor Atiqur Rahman |
Scheme | Medical Research Support Program (MRSP) |
Role | Lead |
Funding Start | 2017 |
Funding Finish | 2017 |
GNo | G1701220 |
Type Of Funding | C2400 – Aust StateTerritoryLocal – Other |
Category | 2400 |
UON | Y |
20163 grants / $1,364,959
Galectin-3 and phagocyte function in severe asthma$718,249
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Professor Jodie Simpson, Doctor Katie Baines, Professor Jay Horvat, Dr Johan Bylund |
Scheme | Project Grant |
Role | Investigator |
Funding Start | 2016 |
Funding Finish | 2018 |
GNo | G1500194 |
Type Of Funding | Aust Competitive - Commonwealth |
Category | 1CS |
UON | Y |
How the placental protein Syncytin impairs maternal immune responses to influenza$626,710
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Conjoint Professor Peter Wark, Laureate Professor Roger Smith, Professor Jay Horvat |
Scheme | Project Grant |
Role | Investigator |
Funding Start | 2016 |
Funding Finish | 2018 |
GNo | G1500388 |
Type Of Funding | Aust Competitive - Commonwealth |
Category | 1CS |
UON | Y |
Emlyn and Jennie Thomas Postgraduate Medical Research Scholarship$20,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Miss Bridie Goggins, Professor Simon Keely, Professor Darryl Knight, Professor Jay Horvat |
Scheme | Postgraduate Research Scholarship |
Role | Investigator |
Funding Start | 2016 |
Funding Finish | 2017 |
GNo | G1600721 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
20153 grants / $84,698
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 |
Investigation of the progression of Alzheimers Disease: Identification of potential drivers of disease$20,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Professor Jay Horvat, Prof LIZ Milward, Professor Phil Hansbro, Dr Daniel Johnstone |
Scheme | Project Grant |
Role | Lead |
Funding Start | 2015 |
Funding Finish | 2015 |
GNo | G1500589 |
Type Of Funding | Grant - Aust Non Government |
Category | 3AFG |
UON | Y |
Greaves Family Postgraduate Scholarship in Medical Research$10,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Professor Jay Horvat, Doctor Richard Kim, Mr James Pinkerton, Professor Phil Hansbro |
Scheme | Postgraduate Research Scholarship |
Role | Lead |
Funding Start | 2015 |
Funding Finish | 2015 |
GNo | G1501396 |
Type Of Funding | Grant - Aust Non Government |
Category | 3AFG |
UON | Y |
20145 grants / $1,665,761
Investigating the role of microbiomes in COPD$822,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Conjoint Professor Peter Wark, Professor Jay Horvat, Professor Philip Hansbro |
Scheme | Project Grant |
Role | Investigator |
Funding Start | 2014 |
Funding Finish | 2020 |
GNo | G1400891 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
Interferon epsilon for Chlamydia RTIs $750,487
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Professor Phil Hansbro, Professor Jay Horvat, Professor Paul Hertzog |
Scheme | Project Grant |
Role | Investigator |
Funding Start | 2014 |
Funding Finish | 2017 |
GNo | G1300071 |
Type Of Funding | Aust Competitive - Commonwealth |
Category | 1CS |
UON | Y |
JuLI Stage $71,674
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Professor Pradeep Tanwar, Professor Eileen McLaughlin, Emeritus Professor Robin Callister, Professor Xu Dong Zhang, Professor Murray Cairns, Professor Brett Nixon, Professor Hubert Hondermarck, Associate Professor Phillip Dickson, Associate Professor Nikki Verrills, Professor Matt Dun, Doctor Jessie Sutherland, Doctor Janani Kumar, Professor Jay Horvat, Associate Professor Susan Hua, Prof LIZ Milward, Associate Professor Estelle Sontag, Professor Dirk Van Helden, Doctor Janet Bristow, Doctor Jean-Marie Sontag |
Scheme | Equipment Grant |
Role | Investigator |
Funding Start | 2014 |
Funding Finish | 2014 |
GNo | G1500860 |
Type Of Funding | Other Public Sector - Commonwealth |
Category | 2OPC |
UON | Y |
The role of the microbiome in the development of food allergy$20,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Professor Simon Keely, Professor Jay Horvat |
Scheme | Project Grant |
Role | Investigator |
Funding Start | 2014 |
Funding Finish | 2014 |
GNo | G1301344 |
Type Of Funding | Grant - Aust Non Government |
Category | 3AFG |
UON | Y |
Thoracic Society of Australia and New Zealand Annual Scientific Meeting, Adelaide AUS, 4-9 April 2014$1,600
Funding body: University of Newcastle - Faculty of Health and Medicine
Funding body | University of Newcastle - Faculty of Health and Medicine |
---|---|
Project Team | Professor Jay Horvat |
Scheme | Travel Grant |
Role | Lead |
Funding Start | 2014 |
Funding Finish | 2014 |
GNo | G1400305 |
Type Of Funding | Internal |
Category | INTE |
UON | Y |
20134 grants / $404,956
Elucidating the mechanisms of infection-induced, steroid-resistant asthma$348,071
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Professor Jay Horvat |
Scheme | Project Grant |
Role | Lead |
Funding Start | 2013 |
Funding Finish | 2015 |
GNo | G1200073 |
Type Of Funding | Aust Competitive - Commonwealth |
Category | 1CS |
UON | Y |
Leica TP 1020 Automatic Tissue Processor for histology applications$35,000
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Professor Pradeep Tanwar, Professor Eileen McLaughlin, Professor Xu Dong Zhang, Conjoint Professor Robert Callister, Associate Professor Phillip Dickson, Professor Hubert Hondermarck, Doctor Jean-Marie Sontag, Professor Dirk Van Helden, Associate Professor Doug Smith, Associate Professor Phil Jobling, Associate Professor Estelle Sontag, Associate Professor Paul Tooney, Associate Professor Susan Hua, Doctor Janet Bristow, Professor Jay Horvat, Prof LIZ Milward, Professor Adam McCluskey, Professor Brett Nixon, Associate Professor Rebecca Lim, Professor Alan Brichta |
Scheme | Equipment Grant |
Role | Investigator |
Funding Start | 2013 |
Funding Finish | 2013 |
GNo | G1201185 |
Type Of Funding | Other Public Sector - Commonwealth |
Category | 2OPC |
UON | Y |
DP73 Digital colour and monochrome camera + cellSens software + Xcite120 fluorescence lamp illuminator$20,000
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Professor Paul Foster, Doctor Alan Hsu, Professor Phil Hansbro, Professor Joerg Mattes, Doctor Katie Baines, Professor Jodie Simpson, Professor Rakesh Kumar, Doctor Nicole Hansbro, Doctor Steven Maltby, Associate Professor Ming Yang, Doctor Gerard Kaiko, Professor Jay Horvat, Professor Simon Keely, Doctor Andrew Jarnicki, Doctor Michael Fricker |
Scheme | Equipment Grant |
Role | Investigator |
Funding Start | 2013 |
Funding Finish | 2013 |
GNo | G1201186 |
Type Of Funding | Other Public Sector - Commonwealth |
Category | 2OPC |
UON | Y |
Thoracic Society of Australia & New Zealand ASM, Darwin Convention Centre, 22 - 27 March 2013$1,885
Funding body: University of Newcastle - Faculty of Health and Medicine
Funding body | University of Newcastle - Faculty of Health and Medicine |
---|---|
Project Team | Professor Jay Horvat |
Scheme | Travel Grant |
Role | Lead |
Funding Start | 2013 |
Funding Finish | 2013 |
GNo | G1300883 |
Type Of Funding | Internal |
Category | INTE |
UON | Y |
20123 grants / $66,500
SpectraMax M5e Multi-Mode Microplate Reader$50,000
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Professor Paul Foster, Professor Phil Hansbro, Professor Joerg Mattes, Professor Rakesh Kumar, Doctor Nicole Hansbro, Associate Professor Ming Yang, Professor Jay Horvat, Professor Simon Keely, Doctor Andrew Jarnicki, Doctor Linda Howland, Dr KELLY Asquith |
Scheme | Equipment Grant |
Role | Investigator |
Funding Start | 2012 |
Funding Finish | 2012 |
GNo | G1100975 |
Type Of Funding | Other Public Sector - Commonwealth |
Category | 2OPC |
UON | Y |
Elucidating the mechanisms of steroid-resistant asthma$15,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Professor Jay Horvat, Professor Phil Hansbro, Professor Paul Foster |
Scheme | Research Grant |
Role | Lead |
Funding Start | 2012 |
Funding Finish | 2012 |
GNo | G1200190 |
Type Of Funding | Contract - Aust Non Government |
Category | 3AFC |
UON | Y |
Thoracic Society of Australia and New Zealand, Canberra, 31 March - 4 April 2012$1,500
Funding body: University of Newcastle - Faculty of Health and Medicine
Funding body | University of Newcastle - Faculty of Health and Medicine |
---|---|
Project Team | Professor Jay Horvat |
Scheme | Travel Grant |
Role | Lead |
Funding Start | 2012 |
Funding Finish | 2013 |
GNo | G1200427 |
Type Of Funding | Internal |
Category | INTE |
UON | Y |
20113 grants / $61,625
SCIREQ FlexiVentFX system + FlexiVentFX extension$45,000
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Professor Phil Hansbro, Professor Paul Foster, Professor Joerg Mattes, Professor Simon Keely, Professor Jay Horvat, Doctor Nicole Hansbro, Associate Professor Ming Yang, Doctor Catherine Ptaschinski, Dr KELLY Asquith, Doctor Gough Au, Conjoint Professor Peter Wark, Distinguished Emeritus Professor John Aitken, Conjoint Professor Keith Jones, Laureate Professor Roger Smith, Professor Judith Black, Professor Rakesh Kumar, Professor Paul Hertzog |
Scheme | Equipment Grant |
Role | Investigator |
Funding Start | 2011 |
Funding Finish | 2011 |
GNo | G1100037 |
Type Of Funding | Other Public Sector - Commonwealth |
Category | 2OPC |
UON | Y |
Antioxidant therapies for suppressing infection-induced asthma in children$15,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Professor Jay Horvat, Professor Lisa Wood, Professor Phil Hansbro |
Scheme | Youth Research Project Grant |
Role | Lead |
Funding Start | 2011 |
Funding Finish | 2011 |
GNo | G1001002 |
Type Of Funding | Contract - Aust Non Government |
Category | 3AFC |
UON | Y |
Thoracic Society of Australia & New Zealand ASM 2011, Perth Convention & Exhibition Centre, Perth WA, 2-4 April 2011$1,625
Funding body: University of Newcastle - Faculty of Health and Medicine
Funding body | University of Newcastle - Faculty of Health and Medicine |
---|---|
Project Team | Professor Jay Horvat |
Scheme | Travel Grant |
Role | Lead |
Funding Start | 2011 |
Funding Finish | 2012 |
GNo | G1100399 |
Type Of Funding | Internal |
Category | INTE |
UON | Y |
20101 grants / $25,000
Improved Treatment Strategies for Infection-Induced Neutrophilic Asthma$25,000
Funding body: Asthma Foundation of New South Wales
Funding body | Asthma Foundation of New South Wales |
---|---|
Project Team | Professor Jay Horvat |
Scheme | Research Grant |
Role | Lead |
Funding Start | 2010 |
Funding Finish | 2010 |
GNo | G0900078 |
Type Of Funding | Grant - Aust Non Government |
Category | 3AFG |
UON | Y |
20093 grants / $24,682
Immunisation against chlamydia-associated asthma$18,182
Funding body: Rebecca L Cooper Medical Research Foundation Ltd
Funding body | Rebecca L Cooper Medical Research Foundation Ltd |
---|---|
Project Team | Professor Jay Horvat, Professor Phil Hansbro, Professor Paul Foster |
Scheme | Research Grant |
Role | Lead |
Funding Start | 2009 |
Funding Finish | 2009 |
GNo | G0189629 |
Type Of Funding | Grant - Aust Non Government |
Category | 3AFG |
UON | Y |
PULSE Education Prize$4,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Professor Jay Horvat |
Scheme | PULSE Education Prize |
Role | Lead |
Funding Start | 2009 |
Funding Finish | 2009 |
GNo | G0189892 |
Type Of Funding | Contract - Aust Non Government |
Category | 3AFC |
UON | Y |
American Association of Immunologists and American Thoracic Society, Seattle USA, 8-21 May 2009$2,500
Funding body: University of Newcastle - Faculty of Health and Medicine
Funding body | University of Newcastle - Faculty of Health and Medicine |
---|---|
Project Team | Professor Jay Horvat |
Scheme | Travel Grant |
Role | Lead |
Funding Start | 2009 |
Funding Finish | 2009 |
GNo | G0190127 |
Type Of Funding | Internal |
Category | INTE |
UON | Y |
20041 grants / $5,000
Modulation of asthma by chlamydial infection at different ages$5,000
Funding body: Asthma Foundation of New South Wales
Funding body | Asthma Foundation of New South Wales |
---|---|
Project Team | Professor Jay Horvat, Professor Phil Hansbro, Conjoint Professor Kenneth Beagley |
Scheme | PhD Scholarships |
Role | Lead |
Funding Start | 2004 |
Funding Finish | 2004 |
GNo | G0183717 |
Type Of Funding | Donation - Aust Non Government |
Category | 3AFD |
UON | Y |
Research Supervision
Number of supervisions
Current Supervision
Commenced | Level of Study | Research Title | Program | Supervisor Type |
---|---|---|---|---|
2024 | PhD | Examining the Effects of Air Pollution on the Central Nervous System | PhD (Human Physiology), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2023 | PhD | Understanding How Obesity And Nutrient Excess Promotes Severe Lung Disease. | PhD (Nutritional Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2023 | PhD | Understanding the Mechanism of Exacerbation of Asthma | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2023 | PhD | Investigating The Gut - Lung Axis In Respiratory Infections In Inflammatory Bowel Disease | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2023 | PhD | Development of novel CAR T Therapies for Children Diagnosed with Central Nervous System Cancers | PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2023 | PhD | Treating Monogenic Diseases (Cystic Fibrosis, Polycystic Kidney Diseases) Using Patients' Organoids As A Disease Model And RNA Therapies As The Treatment. | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2022 | PhD | Quantitative Nondestructive Assessment of Paenibacillus Larvae in Apis Mellifera Hives | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2022 | PhD | Immune Mechanisms Involved in Tolerance and Rejection in Transplant Recipients | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2022 | PhD | Improved Monitoring of Particulate Matter in the Hunter Valley Using Low-Cost Air Quality Sensors | PhD (Environmental Sc), College of Engineering, Science and Environment, The University of Newcastle | Co-Supervisor |
2022 | PhD | Development of an Accurate Biological Test for the Monitoring and Assessment of Occupational Dust Inhalation in High Dust Industries | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2022 | PhD | Neoantigen Immunopeptidomics for the Development of Immunotherapies for the Treatment of Diffuse Intrinsic Pontine Glioma | PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2021 | PhD | Investigation and Therapeutic Manipulation of Iron Uptake Responses in Respiratory Disease | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2020 | PhD | The Role and Therapeutic Targeting of Novel Host Immune Factors in Viral Infection-induced Respiratory Disease | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2020 | PhD | Investigating the Role and Therapeutic Manipulation of Female Sex Hormones in Asthma | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
Past Supervision
Year | Level of Study | Research Title | Program | Supervisor Type |
---|---|---|---|---|
2024 | PhD | Examining Changes in the Neural Control of Respiration Following Early Life Inflammation | PhD (Human Physiology), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2023 | PhD | Characterisation of the Immune Cell-microbiome Interaction within the Gut-lung Axis in Cigarette Smoke Induced Experimental COPD | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2022 | PhD | Characterizing the Effects of Mining Dust Particulate Matter Exposure on Respiratory Health | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2022 | PhD | Understanding the Molecular Mechanisms of Chronic Respiratory Diseases through MultiOmics Approaches | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2022 | PhD | Effects of Chlamydia Infection on Immune Responses in the Central Nervous System and in Multiple Sclerosis | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2022 | PhD | The Role of Inflammasomes during Chlamydia Infection | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2022 | PhD | Investigating New Treatments for Chronic Obstructive Pulmonary Disease | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2022 | PhD | Investigating Asthma-COPD Overlap Using Mouse Models | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2021 | PhD | Characterising the Immunopathology of Functional Dyspepsia | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2021 | PhD | Studies of Respiratory Chlamydia Infections in Mouse Models of Chlamydia Infection and Alzheimer’s Disease | PhD (Medical Genetics), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2021 | PhD | Characterization of Physiological and Neural Alterations in Chlamydial Reproductive Tract Infection | PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2020 | PhD | The Roles of Mast Cells and Mast Cell Proteases During Chlamydia Reproductive Tract Infection | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2019 | PhD | Dietary Fatty Acids and Innate Immune Responses in Primary Human Lung Cells | 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 |
2019 | PhD | In Vitro And in Vivo Investigations of the a-Integrins Regulated by Hypoxia Inducible Factor (HIF)-1 Signalling during Mucosal Wound Healing | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2019 | PhD | Contribution of Cell Death to the Pathogenesis of Chronic Obstructive Pulmonary Disease (COPD) | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2018 | PhD | Elucidating the Mechanisms of Steroid-Resistant Asthma | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal 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 |
2018 | PhD | Role of Iron in the Pathogenesis of Lung Disease | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2017 | PhD | The Role of Interferon Epsilon in Protection Against Chlamydial Reproductive Tract Infections | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2017 | PhD | Mechanisms of Predisposition to Secondary Bacterial Pneumonia | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2017 | PhD | Identification of Novel Therapeutics for Chronic Obstructive Pulmonary Disease | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2017 | PhD | Mechanisms of Lung Inflammation Associated with Inflammatory Bowel 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 |
2016 | PhD | Role of Fibulin-1 in the Pathogenesis of Chronic Pulmonary Diseases | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2015 | PhD | Investigation of the Mechanisms of Respiratory Infection- Induced Lung Disease | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2014 | PhD | Immune Mechanisms that Underpin Early-Life Chlamydia Respiratory Infection-Induced Chronic Lung Disease | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
News
News • 15 Jan 2024
$3.6m NHMRC funding fuels innovative ideas
Premature birth, severe asthma and sperm stress will be a key focus for innovative researchers from the University of Newcastle and Hunter Medical Research Institute (HMRI), who were successful in the latest round of National Health and Medical Research Council (NHMRC) Ideas Grants.
News • 1 Jun 2020
Major funding boost to explore the health impacts of recent bushfires
Researchers from the University of Newcastle, Hunter Medical Research Institute and Hunter New England Health have excelled in the latest round of National Health and Medical Research Council (NHMRC) funding, attracting more than $860,000 to analyse the physiological and mental health effects of hazardous bushfire smoke.
News • 27 Mar 2020
High levels of iron in the lung linked to increased asthma severity
A new study, led by Jay Horvat, Associate Professor of Immunology and Microbiology at the University of Newcastle and HMRI Australia, is the first to show a relationship between iron build up in the lung cells and tissues and the severity of asthma.
News • 1 Mar 2013
Newcastle researchers help in fight against STDs
Newcastle researchers have contributed to the discovery of a protein in the female reproductive tract that protects against sexually transmitted diseases (STDs) such as chlamydia and herpes simplex virus (HSV).
Professor Jay Horvat
Position
Professor
Inflammation and infection-induced diseases research group
School of Biomedical Sciences and Pharmacy
College of Health, Medicine and Wellbeing
Focus area
Immunology and Microbiology
Contact Details
jay.horvat@newcastle.edu.au | |
Phone | (02) 40 420220 |
Fax | (02) 40 420026 |
Office
Room | Level 2, East Wing HMRI Building. |
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Building | HMRI Building |
Location | Other , |