Dr Gang Liu is a lecturer and researcher in respiratory and gastrointestinal tract diseases, and majorly focusing on fibrosis and remodelling. Dr Liu completed his science degree in China (2008) and obtained his Master of Science in Biotechnology in University of Wollongong (2011). He finished PhD the University of Newcastle in 2016. He did his postdoc in Priority Research Centre for Healthy Lung at University of Newcastle from 2016-2017. He then moved to gut disease research as a postdoctoral fellow at Priority Research Centre for Digestive Health and Neurogastroenterology at Hunter Medical Research Institute and University of Newcastle from 2017-2019.
Can supervise: YES
My PhD is focus on airway remodelling and lung fibrosis in severe asthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF). Many factors cause lung remodelling in the three chronic respiratory diseases associate, and the most important feature is abnormal disposition of extracellular matrix (ECM) protein, such as collagen. Fibulin-1 (Fbln1) is a member of ECM proteins, I found that inhibition of Fbln1 expression in mouse by gene knockout and knockdown remarkably reduced lung fibrosis in the diseases. It suggests that Fbln1 may be a new therapeutic target to lung remodelling.
Lung and gut are the tissues that have similar mucosal structure. After my PhD, I extended my fibrosis and ECM research to gut diseases, such as inflammatory bowel disease (IBD) using experimental models of colitis in mice and clinical samples. I also try to understand gut and lung crosstalk and microbiota changes between these two organs during diseases.
Now, I try to understand the mechanisms of fibrosis/remodelling in different organs under disease conditions using in vivo and in vitro models. I will also explore new therapeutic options to fibrotic diseases
Ali, MK, Kim, RY, Brown, AC, Mayall, JR, Karim, R, Pinkerton, JW, Liu, G, Martin, KL, Starkey, MR, Pillar, A, Donovan, C, Pathinayake, PS, Carroll, OR, Trinder, D, Tay, HL, Badi, YE, Kermani, NZ, Guo, Y-K, Aryal, R, Mumby, S, Pavlidis, S, Adcock, IM, Weaver, J, Xenaki, D, Oliver, BG, Holliday, EG, Foster, PS, Wark, PA, Johnstone, DM, Milward, EA, Hansbro, PM & Horvat, JC 2020, 'Crucial role for lung iron level and regulation in the pathogenesis and severity of asthma.', The European respiratory journal.View/Download from: Publisher's site
Accumulating evidence highlights links between iron regulation and respiratory disease. Here, we assessed the relationship between iron levels and regulatory responses in clinical and experimental asthma.We show that cell-free iron levels are reduced in the bronchoalveolar lavage (BAL) supernatant of severe or mild-moderate asthma patients and correlate with lower forced expiratory volume in 1 s (FEV1). Conversely, iron-loaded cell numbers were increased in BAL in these patients and with lower FEV1/forced vital capacity (FEV1/FVC). The airway tissue expression of the iron sequestration molecules divalent metal transporter 1 (DMT1) and transferrin receptor 1 (TFR1) are increased in asthma with TFR1 expression correlating with reduced lung function and increased type 2 (T2) inflammatory responses in the airways. Furthermore, pulmonary iron levels are increased in a house dust mite (HDM)-induced model of experimental asthma in association with augmented Tfr1 expression in airway tissue, similar to human disease. We show that macrophages are the predominant source of increased Tfr1 and Tfr1+ macrophages have increased Il13 expression. We also show that increased iron levels induce increased pro-inflammatory cytokine and/or extracellular matrix (ECM) responses in human airway smooth muscle (ASM) cells and fibroblasts ex vivo and induce key features of asthma, including airway hyper-responsiveness and fibrosis and T2 inflammatory responses, in vivoTogether these complementary clinical and experimental data highlight the importance of altered pulmonary iron levels and regulation in asthma, and the need for a greater focus on the role and potential therapeutic targeting of iron in the pathogenesis and severity of disease.
Ali, MK, Kim, RY, Brown, AC, Donovan, C, Vanka, KS, Mayall, JR, Liu, G, Pillar, AL, Jones-Freeman, B, Xenaki, D, Borghuis, T, Karim, R, Pinkerton, JW, Aryal, R, Heidari, M, Martin, KL, Burgess, JK, Oliver, BG, Trinder, D, Johnstone, DM, Milward, EA, Hansbro, PM & Horvat, JC 2020, 'Critical role for iron accumulation in the pathogenesis of fibrotic lung disease.', The Journal of pathology.View/Download from: Publisher's site
Increased iron levels and/or dysregulated iron homeostasis occurs in several lung diseases. Here, the effects of iron accumulation on the pathogenesis of pulmonary fibrosis and associated lung function decline was investigated using a combination of murine models of iron overload and bleomycin-induced pulmonary fibrosis, primary human lung fibroblasts treated with iron and histological samples from patients with or without idiopathic pulmonary fibrosis (IPF). Iron levels are significantly increased in iron overloaded transferrin receptor 2 (Tfr2) mutant mice and homeostatic iron regulator (Hfe) gene-deficient mice and this is associated with increases in airways fibrosis and reduced lung function. Furthermore, fibrosis and lung function decline are associated with pulmonary iron accumulation in bleomycin-induced pulmonary fibrosis. We also show that iron accumulation is increased in lung sections from IPF patients and that human lung fibroblasts show greater proliferation, and cytokine and extracellular matrix responses when exposed to increased iron levels. Significantly, we show that intranasal treatment with the iron chelator, deferoxamine (DFO), from the time when pulmonary iron levels accumulate, prevents airway fibrosis and decline in lung function in experimental pulmonary fibrosis. Pulmonary fibrosis is associated with an increase in Tfr1+ macrophages that display altered phenotype in disease and DFO treatment modified the abundance of these cells. These experimental and clinical data demonstrate that increased accumulation of pulmonary iron plays a key role in the pathogenesis of pulmonary fibrosis and lung function decline. Furthermore, these data highlight the potential for the therapeutic targeting of increased pulmonary iron in the treatment of fibrotic lung diseases such as IPF. This article is protected by copyright. All rights reserved.
Li, J, Xu, X, Jiang, Y, Hansbro, NG, Hansbro, PM, Xu, J & Liu, G 2020, 'Elastin is a key factor of tumor development in colorectal cancer.', BMC cancer, vol. 20, no. 1, p. 217.View/Download from: Publisher's site
BACKGROUND:Colorectal cancer (CRC) is the most common cancer and a leading cause of death worldwide. Extracellular matrix (ECM) proteins regulate tumor growth and development in CRC. Elastin (ELN) is a component of ECM proteins involved in the tumor microenvironment. However, the role of ELN in CRC remains unclear. METHODS:In this study, we analyzed ELN gene expression in tumors from CRC patients and adjacent non-tumor colon tissues and healthy controls from two existing microarray datasets. ELN protein was measured in human normal colon cells and colon cancer epithelial cells and tumor development was assessed in colon epithelial cells cultured in medium with or without ELN peptide on plates coated with ELN recombinant protein. Control plates were coated with PBS only. RESULTS:We found ELN gene expression was increased in tumors from CRC patients compared to adjacent non-tumor tissues and healthy controls. ELN protein was increased in cancer cells compared to normal colon epithelial cells. Transforming growth factor beta (TGF-β) was a key cytokine to induce production of ECM proteins, but it did not induce ELN expression in colon cancer cells. Matrix metalloproteinase 9 (MMP9) gene expression was increased, but that of MMP12 (elastase) did not change between CRC patients and control. Tissue inhibitor of metalloproteinases 3 (TIMP3) gene expression was decreased in colon tissues from CRC patients compared to healthy controls. However, MMP9, MMP12 and TIMP3 proteins were increased in colon cancer cells. ELN recombinant protein increased proliferation and wound healing in colon cancer epithelial cells. This had further increased in cancer cells incubated in plates coated with recombinant ELN coated plate and in culture media containing ELN peptide. A potential mechanism was that ELN induced epithelial mesenchymal transition with increased alpha-smooth muscle actin and vimentin proteins but decreased E-cadherin protein. Tumor necrosis factor alpha (TNF) mRNA was als...
Liu, G, Cooley, MA, Jarnicki, AG, Borghuis, T, Nair, PM, Tjin, G, Hsu, AC, Haw, TJ, Fricker, M, Harrison, CL, Jones, B, Hansbro, NG, Wark, PA, Horvat, JC, Argraves, WS, Oliver, BG, Knight, DA, Burgess, JK & Hansbro, PM 2019, 'Fibulin-1c regulates transforming growth factor-beta activation in pulmonary tissue fibrosis', JCI INSIGHT, vol. 4, no. 16.View/Download from: UTS OPUS or Publisher's site
Findlay, AD, Foot, JS, Buson, A, Deodhar, M, Jarnicki, AG, Hansbro, PM, Liu, G, Schilter, H, Turner, CI, Zhou, W & Jarolimek, W 2019, 'Identification and Optimization of Mechanism-Based Fluoroallylamine Inhibitors of Lysyl Oxidase-like 2/3', JOURNAL OF MEDICINAL CHEMISTRY, vol. 62, no. 21, pp. 9874-9889.View/Download from: UTS OPUS or Publisher's site
Liu, G, Mateer, SW, Hsu, A, Goggins, BJ, Tay, H, Mathe, A, Fan, K, Neal, R, Bruce, J, Burns, G, Minahan, K, Maltby, S, Fricker, M, Foster, PS, Wark, PAB, Hansbro, PM & Keely, S 2019, 'Platelet activating factor receptor regulates colitis-induced pulmonary inflammation through the NLRP3 inflammasome.', Mucosal immunology, vol. 12, pp. 862-873.View/Download from: UTS OPUS or Publisher's site
Extra-intestinal manifestations (EIM) are common in inflammatory bowel disease (IBD). One such EIM is sub-clinical pulmonary inflammation, which occurs in up to 50% of IBD patients. In animal models of colitis, pulmonary inflammation is driven by neutrophilic infiltrations, primarily in response to the systemic bacteraemia and increased bacterial load in the lungs. Platelet activating factor receptor (PAFR) plays a critical role in regulating pulmonary responses to infection in conditions, such as chronic obstructive pulmonary disease and asthma. We investigated the role of PAFR in pulmonary EIMs of IBD, using dextran sulfate sodium (DSS) and anti-CD40 murine models of colitis. Both models induced neutrophilic inflammation, with increased TNF and IL-1β levels, bacterial load and PAFR protein expression in mouse lungs. Antagonism of PAFR decreased lung neutrophilia, TNF, and IL-1β in an NLRP3 inflammasome-dependent manner. Lipopolysaccharide from phosphorylcholine (ChoP)-positive bacteria induced NLRP3 and caspase-1 proteins in human alveolar epithelial cells, however antagonism of PAFR prevented NLRP3 activation by ChoP. Amoxicillin reduced bacterial populations in the lungs and reduced NLRP3 inflammasome protein levels, but did not reduce PAFR. These data suggest a role for PAFR in microbial pattern recognition and NLRP3 inflammasome signaling in the lung.
Nair, PM, Starkey, MR, Haw, TJ, Liu, G, Collison, AM, Mattes, J, Wark, PA, Morris, JC, Verrills, NM, Clark, AR, Ammit, AJ & Hansbro, PM 2019, 'Enhancing tristetraprolin activity reduces the severity of cigarette smoke-induced experimental chronic obstructive pulmonary disease', CLINICAL & TRANSLATIONAL IMMUNOLOGY, vol. 8, no. 10.View/Download from: UTS OPUS or Publisher's site
Haw, TJ, Starkey, MR, Pavlidis, S, Fricker, M, Arthurs, AL, Nair, PM, Liu, G, Hanish, I, Kim, RY, Foster, PS, Horvat, JC, Adcock, IM & Hansbro, PM 2018, '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, vol. 314, no. 2, pp. L298-L317.View/Download from: UTS OPUS or Publisher's site
Mateer, SW, Mathe, A, Bruce, J, Liu, G, Maltby, S, Fricker, M, Goggins, BJ, Tay, HL, Marks, E, Burns, G, Kim, RY, Minahan, K, Walker, MM, Callister, RC, Foster, PS, Horvat, JC, Hansbro, PM & Keely, S 2018, 'IL-6 Drives Neutrophil-Mediated Pulmonary Inflammation Associated with Bacteremia in Murine Models of Colitis.', The American journal of pathology, vol. 188, no. 7, pp. 1625-1639.View/Download from: UTS OPUS or Publisher's site
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.
Nair, PM, Starkey, MR, Haw, TJ, Ruscher, R, Liu, G, Maradana, MR, Thomas, R, O'Sullivan, BJ & Hansbro, PM 2018, 'RelB-Deficient Dendritic Cells Promote the Development of Spontaneous Allergic Airway Inflammation', AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, vol. 58, no. 3, pp. 352-365.View/Download from: UTS OPUS or Publisher's site
Hansbro, PM, Kim, RY, Starkey, MR, Donovan, C, Dua, K, Mayall, JR, Liu, G, Hansbro, NG, Simpson, JL, Wood, LG, Hirota, JA, Knight, DA, Foster, PS & Horvat, JC 2017, 'Mechanisms and treatments for severe, steroid-resistant allergic airway disease and asthma.', Immunological reviews, vol. 278, no. 1, pp. 41-62.View/Download from: UTS OPUS or Publisher's site
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.
Liu, G, Cooley, MA, Nair, PM, Donovan, C, Hsu, AC, Jarnicki, AG, Haw, TJ, Hansbro, NG, Ge, Q, Brown, AC, Tay, H, Foster, PS, Wark, PA, Horvat, JC, Bourke, JE, Grainge, CL, Argraves, WS, Oliver, BG, Knight, DA, Burgess, JK & Hansbro, PM 2017, 'Airway remodelling and inflammation in asthma are dependent on the extracellular matrix protein fibulin-1c.', The Journal of Pathology, vol. 243, no. 4, pp. 510-523.View/Download from: UTS OPUS or Publisher's site
Asthma is a chronic inflammatory disease of the airways. It is characterized by allergic airway inflammation, airway remodelling, and airway hyperresponsiveness (AHR). Asthma patients, in particular those with chronic or severe asthma, have airway remodelling that is associated with the accumulation of extracellular matrix (ECM) proteins, such as collagens. Fibulin-1 (Fbln1) is an important ECM protein that stabilizes collagen and other ECM proteins. The level of Fbln1c, one of the four Fbln1 variants, which predominates in both humans and mice, is increased in the serum and airways fluids in asthma but its function is unclear. We show that the level of Fbln1c was increased in the lungs of mice with house dust mite (HDM)-induced chronic allergic airway disease (AAD). Genetic deletion of Fbln1c and therapeutic inhibition of Fbln1c in mice with chronic AAD reduced airway collagen deposition, and protected against AHR. Fbln1c-deficient (Fbln1c-/- ) mice had reduced mucin (MUC) 5 AC levels, but not MUC5B levels, in the airways as compared with wild-type (WT) mice. Fbln1c interacted with fibronectin and periostin that was linked to collagen deposition around the small airways. Fbln1c-/- mice with AAD also had reduced numbers of α-smooth muscle actin-positive cells around the airways and reduced airway contractility as compared with WT mice. After HDM challenge, these mice also had fewer airway inflammatory cells, reduced interleukin (IL)-5, IL-13, IL-33, tumour necrosis factor (TNF) and CXCL1 levels in the lungs, and reduced IL-5, IL-33 and TNF levels in lung-draining lymph nodes. Therapeutic targeting of Fbln1c reduced the numbers of GATA3-positive Th2 cells in the lymph nodes and lungs after chronic HDM challenge. Treatment also reduced the secretion of IL-5 and IL-13 from co-cultured dendritic cells and T cells restimulated with HDM extract. Human epithelial cells cultured with Fbln1c peptide produced more CXCL1 mRNA than medium-treated controls. Our data show that...
Jones, B, Donovan, C, Liu, G, Gomez, HM, Chimankar, V, Harrison, CL, Wiegman, CH, Adcock, IM, Knight, DA, Hirota, JA & Hansbro, PM 2017, 'Animal models of COPD: What do they tell us?', Respirology, vol. 22, no. 1, pp. 21-32.View/Download from: UTS OPUS or Publisher's site
COPD is a major cause of global mortality and morbidity but current treatments are poorly effective. This is because the underlying mechanisms that drive the development and progression of COPD are incompletely understood. Animal models of disease provide a valuable, ethically and economically viable experimental platform to examine these mechanisms and identify biomarkers that may be therapeutic targets that would facilitate the development of improved standard of care. Here, we review the different established animal models of COPD and the various aspects of disease pathophysiology that have been successfully recapitulated in these models including chronic lung inflammation, airway remodelling, emphysema and impaired lung function. Furthermore, some of the mechanistic features, and thus biomarkers and therapeutic targets of COPD identified in animal models are outlined. Some of the existing therapies that suppress some disease symptoms that were identified in animal models and are progressing towards therapeutic development have been outlined. Further studies of representative animal models of human COPD have the strong potential to identify new and effective therapeutic approaches for COPD.
Nair, PM, Starkey, MR, Haw, TJ, Liu, G, Horvat, JC, Morris, JC, Verrills, NM, Clark, AR, Ammit, AJ & Hansbro, PM 2017, 'Targeting PP2A and proteasome activity ameliorates features of allergic airway disease in mice.', Allergy, vol. 72, no. 12, pp. 1891-1903.View/Download from: UTS OPUS or Publisher's site
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.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.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.These findings highlight the potential of combination therapies that enhance PP2A and inhibit proteasome activity as novel therapeutic strategies for asthma.
Gold, MJ, Hiebert, PR, Park, HY, Stefanowicz, D, Le, A, Starkey, MR, Deane, A, Brown, AC, Liu, G, Horvat, JC, Ibrahim, ZA, Sukkar, MB, Hansbro, PM, Carlsten, C, VanEeden, S, Sin, DD, McNagny, KM, Knight, DA & Hirota, JA 2016, 'Mucosal production of uric acid by airway epithelial cells contributes to particulate matter-induced allergic sensitization.', Mucosal Immunology, vol. 9, no. 3, pp. 809-820.View/Download from: UTS OPUS or Publisher's site
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. PM10 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). PM10-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.
Haw, TJ, Starkey, MR, Nair, PM, Pavlidis, S, Liu, G, Nguyen, DH, Hsu, AC, Hanish, I, Kim, RY, Collison, AM, Inman, MD, Wark, PA, Foster, PS, Knight, DA, Mattes, J, Yagita, H, Adcock, IM, Horvat, JC & Hansbro, PM 2016, 'A pathogenic role for tumor necrosis factor-related apoptosis-inducing ligand in chronic obstructive pulmonary disease', MUCOSAL IMMUNOLOGY, vol. 9, no. 4, pp. 859-872.View/Download from: Publisher's site
Jarnicki, AG, Schilter, H, Liu, G, Wheeldon, K, Essilfie, A-T, Foot, JS, Yow, TT, Jarolimek, W & Hansbro, PM 2016, 'The inhibitor of semicarbazide-sensitive amine oxidase, PXS-4728A, ameliorates key features of chronic obstructive pulmonary disease in a mouse model', BRITISH JOURNAL OF PHARMACOLOGY, vol. 173, no. 22, pp. 3161-3175.View/Download from: Publisher's site
Liu, G, Cooley, MA, Jarnicki, AG, Hsu, AC-Y, Nair, PM, Haw, TJ, Fricker, M, Gellatly, SL, Kim, RY, Inman, MD, Tjin, G, Wark, PAB, Walker, MM, Horvat, JC, Oliver, BG, Argraves, WS, Knight, DA, Burgess, JK & Hansbro, PM 2016, 'Fibulin-1 regulates the pathogenesis of tissue remodeling in respiratory diseases', JCI INSIGHT, vol. 1, no. 9.View/Download from: UTS OPUS or Publisher's site
Liu, G, Mateer, S, Mathe, A, Goggins, B, Hsu, A, Minahan, K, Bruce, J, Fricker, M, Wark, P, Hansbro, P & Keely, S 2018, 'Platelet Activating Factor Receptor (PAFR) Regulates Colitis-induced Pulmonary Inflammation', FASEB JOURNAL, Annual Meeting of Amer-Assoc-of-Anatomists (AAA), Amer-Physiol-Soc (APS), Amer-Soc-for-Biochemistry-and-Mol-Biol (ASBMB), Amer-Soc-for-Investigat-Pathol (ASIP), Amer-Soc-for-Pharmacol-and-Experimental-Therapeut (ASPET) on Experimental Biology (EB), FEDERATION AMER SOC EXP BIOL, Amer Assoc Anatomists, San Diego, CA.
Horvat, JC, Ali, MK, Johnstone, D, Kim, RY, Mayall, JR, Karim, R, Pinkerton, JW, Heidari, M, Martin, KL, Donovam, C, Liu, G, Milward, EA & Hansbro, PM 2017, 'Role for dysregulated iron in the pathogenesis of murine models of lung disease', JOURNAL OF IMMUNOLOGY, Annual Meeting of the American-Association-of-Immunologists (AAI), AMER ASSOC IMMUNOLOGISTS, Washington, DC.