Dr Ming Yang

Senior Lecturer

School of Biomedical Sciences and Pharmacy (Immunology and Microbiology)

Career Summary

Biography

Dr. Yang graduated from The John Curtin School of Medical Research, Institute of Advanced Studies, Australian National University, with distinction: he was awarded the prestigious Frank Fenner Medal for the  most  outstanding  PhD  dissertation.  Subsequently he was awarded  a prestigious University of Newcastle Research Fellowship and was promoted to level B within the first year after graduation.  Based on his research directions and productivity, he was awarded an NHMRC New Investigator grant. In 2012, he was promoted to Senior Research Fellow. He is now internationally known for his investigations into the pathogenesis of asthma, and the molecular and cellular regulation of inflammation.

Dr. Yang’s group has received international recognition through publication in leading biomedical science journals and has contributed to more than 30 refereed manuscripts in high impact journals (J Exp Med, J Clin Invest, Gastroenterology, J Allergy Clin Immunology, PNAS, J Immunology) with more than 1500 combined citations. He has been successful in obtaining research grants both independently and in collaboration with other investigators (over $3.8 Million). 

Research Directions and Significant Achievements:

In recent years Dr. Yang has initiated investigations into the mechanisms that regulate steroid resistant inflammatory pathways in the lung, to help understand how steroid resistance may develop in asthma. Understanding the mechanisms that regulate steroid-resistant inflammation is important and developing novel non- steroidal therapeutic approaches to the disease will be highly beneficial, as these patients suffer greater morbidity and mortality. Currently, there is no effective treatment and there is very limited functional evidence of the way in which the inflammatory pathways are activated in these patients. Building on clinical studies, we have recently demonstrated, for the first time, that macrophages are crucial in regulating steroid-resistant inflammatory signals. Two papers have been published in the Journal of Immunology and their significance has been recognised by the American Academy of Asthma Allergy and Immunology (symposium invitation, 2010) and the invitation to write two reviews for Current Drug Targets and Journal of Leukocyte Biology.

The unique complexity of respiratory system has limited the development of therapeutic agents that show clinical benefit for severe asthmatic patients. However, the more efficient therapeutics may be developed by silencing the dominant proinflammatory genes, which are responsible for the propagation of the disease. Employing small ‘non-coding’ RNA molecules called microRNAs (miRNA), small interfering RNAs (siRNA) or synthetic analogues of these molecules, ‘antagomirs’, to specifically silence aberrant gene function is of growing interest. Dr. Yang was at the forefront of the first application of RNA interference to modulate AHR and macrophage function in the lung (2006, J Immunology). His works in this field has been recognised by invitations to write reviews for Drug Discovery Today, Pharmacology & Therapeutics and American Journal of Respiratory Cellular and Molecular Biology. Recently, he has been investigating the central roles of miRNA in the regulation of the pro-inflammatory effects of macrophages and thus potential innate immune mediated AHR. Dr. Yang also has extensive research interests in characterizing the pivotal roles of these small non-coding RNAs in modulating the differentiation and function of granulocytes and other immune cells.

Research Expertise
- Immunology - Pharmacology - Pharmaceutical Sciences

Collaborations
Dr. Yang has productive collaborations within Australia and oversea internationally renowned groups. He has extensive academic, intellectual and procedural input into these collaborations and has also contributed significant experimental expertise. These collaborations will continue for the foreseeable future.

Qualifications

  • PhD, Australian National University

Keywords

  • Gene Regulation
  • Haematopoiesis
  • Immunology
  • Infectious Disease
  • Inflammation Inhibition
  • Intracellular Signalling Transduction
  • Pharmaceutical Sciences
  • Pharmacology
  • Respiratory Disease

Fields of Research

Code Description Percentage
310702 Infectious agents 40
320402 Applied immunology (incl. antibody engineering, xenotransplantation and t-cell therapies) 60

Professional Experience

UON Appointment

Title Organisation / Department
Senior Lecturer University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia
Senior Lecturer University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia
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Publications

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


Journal article (66 outputs)

Year Citation Altmetrics Link
2021 Yuan F, Jiang L, Li Q, Sokulsky L, Wanyan Y, Wang L, et al., 'A Selective a7 Nicotinic Acetylcholine Receptor Agonist, PNU-282987, Attenuates ILC2s Activation and Alternaria-Induced Airway Inflammation', Frontiers in Immunology, 11 (2021) [C1]

Background: The anti-inflammatory effect of an a7nAChR agonist, PNU-282987, has previously been explored in the context of inflammatory disease. However, the effects of PNU-282987... [more]

Background: The anti-inflammatory effect of an a7nAChR agonist, PNU-282987, has previously been explored in the context of inflammatory disease. However, the effects of PNU-282987 on type 2 innate lymphoid cells (ILC2s)-mediated allergic airway inflammation has not yet been established. Aims: To determine the effects of PNU-282987 on the function of ILC2s in the context of IL-33¿ or Alternaria Alternata (AA)¿ induced airway inflammation. Methods: PNU-282987 was administered to mice that received recombinant IL-33 or AA intranasal challenges. Lung histological analysis and flow cytometry were performed to determine airway inflammation and the infiltration and activation of ILC2s. The previously published a7nAChR agonist GTS-21 was employed as a comparable reagent. ILC2s were isolated from murine lung tissue and cultured in vitro in the presence of IL-33, IL-2, and IL-7 with/without either PNU-282987 or GTS-21. The expression of the transcription factors GATA3, IKK, and NF-¿B were also determined. Results: PNU-282987 and GTS-21 significantly reduced goblet cell hyperplasia in the airway, eosinophil infiltration, and ILC2s numbers in BALF, following IL-33 or AA challenge. In vitro IL-33 stimulation of isolated lung ILC2s showed a reduction of GATA3 and Ki67 in response to PNU-282987 or GTS-21 treatments. There was a significant reduction in IKK and NF-¿B phosphorylation in the PNU-282987¿treated group when compared to the GTS-21¿treated ILC2s. Conclusion: PNU-282987 inhibits ILC2-associated airway inflammation, where its effects were comparable to that of GTS-21.

DOI 10.3389/fimmu.2020.598165
Co-authors Hock Tay
2021 Duan Z, Liu M, Yuan L, Du X, Wu M, Yang Y, et al., 'Innate lymphoid cells are double-edged swords under the mucosal barrier', JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, (2021)
DOI 10.1111/jcmm.16856
2021 Collison AM, Sokulsky LA, Kepreotes E, Pereira de Siqueira A, Morten M, Edwards MR, et al., 'miR-122 promotes virus-induced lung disease by targeting SOCS1.', JCI Insight, 6 (2021)
DOI 10.1172/jci.insight.127933
Co-authors Nathan Bartlett, Adam Collison, Joerg Mattes, Paul Foster
2021 Wang L, Netto KG, Zhou L, Liu X, Wang M, Zhang G, et al., 'Single-cell transcriptomic analysis reveals the immune landscape of lung in steroid-resistant asthma exacerbation', Proceedings of the National Academy of Sciences of the United States of America, 118 (2021) [C1]

Exaggerated airway hyperresponsiveness and inflammation are hallmarks of asthma, and lipopolysaccharide (LPS) exposure is linked to the severity of the disease and steroid resista... [more]

Exaggerated airway hyperresponsiveness and inflammation are hallmarks of asthma, and lipopolysaccharide (LPS) exposure is linked to the severity of the disease and steroid resistance. To investigate the mechanisms underlying asthma exacerbation, we established a mouse model of LPS-induced steroid-resistant exacerbation on the background of house dust mite (HDM)-induced asthma to profile the immune cells in lung by using single-cell RNA deep sequencing. Twenty immune subsets were identified by their molecular and functional properties. Specific cell clusters of basophils, type 2 innate lymphoid cells (ILC2), and CD8+ memory T cells were the predominant sources of interleukin (IL)-4 and IL-13 transcripts whose expressions were dexamethasone resistant. Production of IL-13 by these cells was validated by IL-13-reporter mice. Neutralization of IL-13 abolished HDM/LPS-induced airway hyperresponsiveness, airway inflammation, and decreased mucus hypersecretion. Furthermore, using Ingenuity Pathway Analysis systems, we identified canonical pathways and upstream regulators that regulate the activation of basophils, ILC2, and CD8+ memory T cells. Our study provides mechanistic insights and an important reference resource for further understanding of the immune landscape during asthma exacerbation.

DOI 10.1073/pnas.2005590118
Citations Scopus - 3Web of Science - 2
Co-authors Paul Foster
2021 Yang Y, Yuan L, Yang M, Du X, Qin L, Wang L, et al., 'Aberrant Methylation of Aging-Related Genes in Asthma', FRONTIERS IN MOLECULAR BIOSCIENCES, 8 (2021) [C1]
DOI 10.3389/fmolb.2021.655285
2021 Li H, Wang H, Sokulsky L, Liu S, Yang R, Liu X, et al., 'Single-cell transcriptomic analysis reveals key immune cell phenotypes in the lungs of patients with asthma exacerbation', Journal of Allergy and Clinical Immunology, 147 941-954 (2021) [C1]

Background: Asthma exacerbations are associated with heightened asthma symptoms, which can result in hospitalization in severe cases. However, the molecular immunologic processes ... [more]

Background: Asthma exacerbations are associated with heightened asthma symptoms, which can result in hospitalization in severe cases. However, the molecular immunologic processes that determine the course of an exacerbation remain poorly understood, impeding the progression of development of effective therapies. Objective: Our aim was to identify candidate genes that are strongly associated with asthma exacerbation at a cellular level. Methods: Subjects with asthma exacerbation and healthy control subjects were recruited, and bronchoalveolar lavage fluid was isolated from these subjects via bronchoscopy. Cells were isolated through fluorescence-activated cell sorting, and single-cell RNA sequencing was performed on enriched cell populations. Results: We showed that the levels of monocytes, CD8+ T cells, and macrophages are significantly elevated in the bronchoalveolar lavage fluid of patients. A set of cytokines and intracellular transduction regulators are associated with asthma exacerbations and are shared across multiple cell clusters, forming a complicated molecular framework. An additional group of core exacerbation-associated modules is activated, including eukaryotic initiation factor 2 signaling, ephrin receptor signaling, and C-X-C chemokine receptor type 4 signaling in the subpopulations of CD8+ T cells (C1-a) and monocyte clusters (C7 clusters), which are associated with infection. Conclusion: Our study identified a significant number of severe asthma¿associated genes that are differentially expressed by multiple cell clusters.

DOI 10.1016/j.jaci.2020.09.032
Citations Scopus - 1Web of Science - 1
2021 Yuan L, Wang L, Du X, Qin L, Yang M, Zhou K, et al., 'The DNA methylation of FOXO3 and TP53 as a blood biomarker of late-onset asthma (vol 18, 467, 2020)', JOURNAL OF TRANSLATIONAL MEDICINE, 19 (2021)
DOI 10.1186/s12967-021-02777-7
2021 Liu X, Nguyen TH, Sokulsky L, Li X, Netto KG, Hsu AC-Y, et al., 'IL-17A is a common and critical driver of impaired lung function and immunopathology induced by influenza virus, rhinovirus and respiratory syncytial virus', RESPIROLOGY, (2021)
DOI 10.1111/resp.14141
Co-authors Alan Hsu, Paul Foster
2020 Yuan L, Wang L, Du X, Qin L, Yang M, Zhou K, et al., 'The DNA methylation of FOXO3 and TP53 as a blood biomarker of late-onset asthma', JOURNAL OF TRANSLATIONAL MEDICINE, 18 (2020) [C1]
DOI 10.1186/s12967-020-02643-y
Citations Scopus - 2Web of Science - 2
2020 Sokulsky LA, Garcia-Netto K, Nguyen TH, Girkin JLN, Collison A, Mattes J, et al., 'A critical role for the CXCL3/CXCL5/CXCR2 neutrophilic chemotactic axis in the regulation of type 2 responses in a model of rhinoviral-induced asthma exacerbation', Journal of Immunology, 205 2468-2478 (2020)
DOI 10.4049/jimmunol.1901350
Citations Scopus - 5Web of Science - 5
Co-authors Paul Foster, Jason Girkin, Joerg Mattes, Nathan Bartlett, Adam Collison, Gerard Kaiko
2020 Sokulsky LA, Goggins B, Sherwin S, Eyers F, Kaiko GE, Board PG, et al., 'GSTO1-1 is an upstream suppressor of M2 macrophage skewing and HIF-1 alpha-induced eosinophilic airway inflammation', CLINICAL AND EXPERIMENTAL ALLERGY, 50 609-624 (2020) [C1]
DOI 10.1111/cea.13582
Citations Scopus - 6Web of Science - 4
Co-authors Simon Keely, Gerard Kaiko, Paul Foster, Bridie Goggins
2020 Wu M, Yang Y, Yuan L, Yang M, Wang L, Du X, et al., 'DNA methylation down-regulates integrin ß4 expression in asthmatic airway epithelial cells', Clinical and Experimental Allergy, 50 1127-1139 (2020) [C1]
DOI 10.1111/cea.13697
Citations Scopus - 1Web of Science - 1
2020 Yuan L, Zhang X, Yang M, Du X, Wang L, Wu S, et al., 'Airway epithelial integrin ß4 suppresses allergic inflammation by decreasing CCL17 production', Clinical Science, 134 1735-1749 (2020) [C1]

Airway epithelial cells (AECs) play a key role in asthma susceptibility and severity. Integrin ß4 (ITGB4) is a structural adhesion molecule that is down-regulated in the airway ep... [more]

Airway epithelial cells (AECs) play a key role in asthma susceptibility and severity. Integrin ß4 (ITGB4) is a structural adhesion molecule that is down-regulated in the airway epithelium of asthma patients. Although a few studies hint toward the role of ITGB4 in asthmatic inflammation pathogenesis, their specific resultant effects remain unexplored. In the present study, we determined the role of ITGB4 of AECs in the regulation of Th2 response and identified the underpinning molecular mechanisms. We found that ITGB4 deficiency led to exaggerated lung inflammation and AHR with higher production of CCL17 in house dust mite (HDM)-treated mice. ITGB4 regulated CCL17 production in AECs through EGFR, ERK and NF-¿B pathways. EFGR-antagonist treatment or the neutralization of CCL17 both inhibited exaggerated pathological marks in HDM-challenged ITGB4-deficient mice. Together, these results demonstrated the involvement of ITGB4 deficiency in the development of Th2 responses of allergic asthma by down-regulation of EGFR and CCL17 pathway in AECs.

DOI 10.1042/CS20191188
Citations Scopus - 1Web of Science - 2
2020 Du X, Yang Y, Xiao G, Yang M, Yuan L, Qin L, et al., 'Respiratory syncytial virus infection-induced mucus secretion by down-regulation of miR-34b/c-5p expression in airway epithelial cells', Journal of Cellular and Molecular Medicine, 24 12694-12705 (2020) [C1]

Severe RSV infection is the main cause of hospitalization to children under the age of five. The regulation of miRNAs on the severity of RSV infection is unclear. The aim of the s... [more]

Severe RSV infection is the main cause of hospitalization to children under the age of five. The regulation of miRNAs on the severity of RSV infection is unclear. The aim of the study was to identify the critical differential expression miRNAs (DE miRNAs) that can regulate the pathological response in RSV-infected airway epithelial cells. In this study, miRNA and mRNA chips of RSV-infected airway epithelia from Gene Expression Omnibus (GEO) were screened and analysed, separately. DE miRNAs-targeted genes were performed for further pathway and process enrichment analysis. DE miRNA-targeted gene functional network was constructed on the basis of miRNA-mRNA interaction. The screened critical miRNA was also investigated by bioinformatics analysis. Then, RSV-infected human bronchial epithelial cells (HBECs) were constructed to verify the expression of the DE miRNAs. Finally, specific synthetic DE miRNAs mimics were used to confirm the effect of DE miRNAs on the RSV-infected HBECs. 45 DE miRNAs were identified from GEO62306 dataset. Our results showed that hsa-mir-34b-5p and hsa-mir-34c-5p decreased significantly in HBECs after RSV infection. Consistent with the biometric analysis, hsa-mir-34b/c-5p is involved in the regulation of mucin expression gene MUC5AC. In RSV-infected HBECs, the inducement of MUC5AC production by decreased hsa-mir-34b/c-5p was partly mediated through activation of c-Jun. These findings provide new insights into the mechanism of mucus obstruction after RSV infection and represent valuable targets for RSV infection and airway obstruction treatment.

DOI 10.1111/jcmm.15845
Citations Scopus - 1Web of Science - 1
2020 Hadjigol S, Netto KG, Maltby S, Tay HL, Nguyen TH, Hansbro NG, et al., 'Lipopolysaccharide induces steroid-resistant exacerbations in a mouse model of allergic airway disease collectively through IL-13 and pulmonary macrophage activation', Clinical and Experimental Allergy, 50 82-94 (2020) [C1]

Background: Acute exacerbations of asthma represent a major burden of disease and are often caused by respiratory infections. Viral infections are recognized as significant trigge... [more]

Background: Acute exacerbations of asthma represent a major burden of disease and are often caused by respiratory infections. Viral infections are recognized as significant triggers of exacerbations; however, less is understood about the how microbial bioproducts such as the endotoxin (lipopolysaccharide (LPS)) trigger episodes. Indeed, increased levels of LPS have been linked to asthma onset, severity and steroid resistance. Objective: The goal of this study was to identify mechanisms underlying bacterial-induced exacerbations by employing LPS as a surrogate for infection. Methods: We developed a mouse model of LPS-induced exacerbation on the background of pre-existing type-2 allergic airway disease (AAD). Results: LPS-induced exacerbation was characterized by steroid-resistant airway hyperresponsiveness (AHR) and an exaggerated inflammatory response distinguished by increased numbers of infiltrating neutrophils/macrophages and elevated production of lung inflammatory cytokines, including TNFa, IFN¿, IL-27 and MCP-1. Expression of the type-2 associated inflammatory factors such as IL-5 and IL-13 were elevated in AAD but not altered by LPS exposure. Furthermore, AHR and airway inflammation were no longer suppressed by corticosteroid (dexamethasone) treatment after LPS exposure. Depletion of pulmonary macrophages by administration of 2-chloroadenosine into the lungs suppressed AHR and reduced IL-13, TNFa and IFN¿ expression. Blocking IL-13 function, through either IL-13-deficiency or administration of specific blocking antibodies, also suppressed AHR and airway inflammation. Conclusions & Clinical Relevance: We present evidence that IL-13 and innate immune pathways (in particular pulmonary macrophages) contribute to LPS-induced exacerbation of pre-existing AAD and provide insight into the complex molecular processes potentially underlying microbial-induced exacerbations.

DOI 10.1111/cea.13505
Citations Scopus - 5Web of Science - 3
Co-authors Hock Tay, Steven Maltby, Paul Foster, Philip Hansbro
2018 Liu C, Yuan L, Zou Y, Yang M, Chen Y, Qu X, et al., 'ITGB4 is essential for containing HDM-induced airway inflammation and airway hyperresponsiveness', Journal of Leukocyte Biology, 103 897-908 (2018) [C1]

Airway epithelial cells play a significant role in the pathogenesis of asthma. Although the structural and functional defects of airway epithelial cells have been postulated to in... [more]

Airway epithelial cells play a significant role in the pathogenesis of asthma. Although the structural and functional defects of airway epithelial cells have been postulated to increase asthma susceptibility and exacerbate asthma severity, the mechanism and implication of these defects remain uncertain. Integrin ß4 (ITGB4) is a structural adhesion molecule that is downregulated in the airway epithelium of asthma patients. In this study, we demonstrated that ITGB4 deficiency leads to severe allergy-induced airway inflammation and airway hyper-responsiveness (AHR) in mice. After house dust mite (HDM) challenge, epithelial cell-specific ITGB4-deleted mice showed increased lymphocyte, eosinophil, and neutrophil infiltration into lung compared with that of the wild-type mice. ITGB4 deficiency also resulted in increased expression of the Th2 cytokine IL-4, IL-13, and the Th17 cytokine IL-17A in the lung tissue and in the T cells after HDM challenge. The aggravated inflammation in ITGB4 defect mice was partly caused by enhanced disrupted epithelial barrier integrity after HDM stress, which induced the increased thymic stromal lymphopoietin secretion from airway epithelial cells. This study therefore demonstrates that ITGB4 plays a pivotal role in containing allergen-mediated lung inflammation and airway hyper-responsiveness in allergic asthma.

DOI 10.1002/JLB.3A1017-411RR
Citations Scopus - 10Web of Science - 11
2018 Thi HN, Liu X, Su ZZ, Hsu AC-Y, Foster PS, Yang M, 'Potential Role of MicroRNAs in the Regulation of Antiviral Responses to influenza infection', FRONTIERS IN IMMUNOLOGY, 9 (2018) [C1]
DOI 10.3389/fimmu.2018.01541
Citations Scopus - 20Web of Science - 19
Co-authors Alan Hsu, Paul Foster
2018 Nguyen TH, Maltby S, Tay HL, Eyers F, Foster PS, Yang M, 'Identification of IFN- and IL-27 as Critical Regulators of Respiratory Syncytial Virus-Induced Exacerbation of Allergic Airways Disease in a Mouse Model', Journal of Immunology, 200 237-247 (2018) [C1]

Respiratory syncytial virus (RSV) infection induces asthma exacerbations, which leads to worsening of clinical symptoms and may result in a sustained decline in lung function. Exa... [more]

Respiratory syncytial virus (RSV) infection induces asthma exacerbations, which leads to worsening of clinical symptoms and may result in a sustained decline in lung function. Exacerbations are the main cause of morbidity and mortality associated with asthma, and significantly contribute to asthma-associated healthcare costs. Although glucocorticoids are used to manage exacerbations, some patients respond to them poorly. The underlying mechanisms associated with steroid-resistant exacerbations remain largely unknown. We have previously established a mouse model of RSV-induced exacerbation of allergic airways disease, which mimics hallmark clinical features of asthma. In this study, we have identified key roles for macrophage IFN-¿ and IL-27 in the regulation of RSV-induced exacerbation of allergic airways disease. Production of IFN-¿ and IL-27 was steroid-resistant, and neutralization of IFN-¿ or IL-27 significantly suppressed RSV-induced steroid-resistant airway hyperresponsiveness and airway inflammation. We have previously implicated activation of pulmonary macrophage by TNF-a and/or MCP-1 in the mechanisms of RSV-induced exacerbation. Stimulation of pulmonary macrophages with TNF-a and/or MCP-1 induced expression of both IFN-¿ and IL-27. Our findings highlight critical roles for IFN-¿ and IL-27, downstream of TNF-a and MCP-1, in the mechanism of RSV-induced exacerbation. Thus, targeting the pathways that these factors activate may be a potential therapeutic approach for virus-induced asthma exacerbations.

DOI 10.4049/jimmunol.1601950
Citations Scopus - 14Web of Science - 13
Co-authors Paul Foster, Steven Maltby, Hock Tay
2016 Nguyen TH, Maltby S, Simpson JL, Eyers F, Baines KJ, Gibson PG, et al., 'TNF-a and macrophages are critical for respiratory syncytial virus-induced exacerbations in a mouse model of allergic airways disease', Journal of Immunology, 196 3547-3558 (2016) [C1]

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

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

DOI 10.4049/jimmunol.1502339
Citations Scopus - 32Web of Science - 33
Co-authors Katherine Baines, Steven Maltby, Peter Gibson, Jodie Simpson, Paul Foster
2016 Xiang Y, Eyers F, Herbert C, Tay HL, Foster PS, Yang M, 'MicroRNA-487b is a negative regulator of macrophage activation by targeting IL-33 production', Journal of Immunology, 196 3421-3428 (2016) [C1]

MicroRNAs (miRNAs) are short noncoding RNAs that regulate a broad spectrum of biological processes, including immune responses. Although the contributions of miRNAs to the functio... [more]

MicroRNAs (miRNAs) are short noncoding RNAs that regulate a broad spectrum of biological processes, including immune responses. Although the contributions of miRNAs to the function of immune cells are beginning to emerge, their specific roles remain largely unknown. IL-33 plays an important role in macrophage activation for innate host defense and proinflammatory responses. In this study, we report that miR-487b can suppress the levels of mRNA and protein for IL-33 during the differentiation of bone marrow-derived macrophages (BMDMs). This results in inhibition of IL-33-induced expression of Ag-presenting and costimulatory molecules and proinflammatory mediators. A luciferase assay showed that miR-487b binds to the IL-33 39-untranslated region. We also confirmed that IL-33 directly promotes the activation of BMDMs by increasing the expression of MHC class I, MHC class II, CD80/CD86, and inducible NO synthase (iNOS) in a dose-dependent manner. Exposure of BMDMs to the TLR4 ligand, LPS, decreased miR-487b expression, increased IL-33 transcript levels, and induced the production of proinflammatory mediators (e.g., iNOS, IL-1b, IL-6, and TNF-a). Treatment with a specific inhibitor of miR-487b function also resulted in increased levels of IL-33 mRNA, which augmented LPS-induced expression of these inflammatory mediators in macrophages. Collectively, our results indicate that miR-487b plays a negative regulatory role in macrophages by controlling the levels of IL-33 transcript and protein to fine-tune innate immune host defense and proinflammatory responses of these cells. Thus, miR-487b plays an important role in the regulation of macrophage homeostasis and activation by targeting IL-33 transcripts.

DOI 10.4049/jimmunol.1502081
Citations Scopus - 26Web of Science - 26
Co-authors Hock Tay, Paul Foster
2016 Zhou H, Zhang J, Eyers F, Xiang Y, Herbert C, Tay HL, et al., 'Identification of the microRNA networks contributing to macrophage differentiation and function', Oncotarget, 7 28806-28820 (2016) [C1]

Limited evidence is available about the specific miRNA networks that regulate differentiation of specific immune cells. In this study, we characterized miRNA expression and associ... [more]

Limited evidence is available about the specific miRNA networks that regulate differentiation of specific immune cells. In this study, we characterized miRNA expression and associated alterations in expression with putative mRNA targets that are critical during differentiation of macrophages. In an effort to map the dynamic changes in the bone marrow (BM), we profiled whole BM cultures during differentiation into macrophages. We identified 112 miRNAs with expression patterns that were differentially regulated 5-fold or more during BMDM development. With TargetScan and MeSH databases, we identified 1267 transcripts involved in 30 canonical pathways linked to macrophage biology as potentially regulated by these specific 112 miRNAs. Furthermore, by employing miRanda and Ingenuity Pathways Analysis (IPA) analysis systems, we identified 18 miRNAs that are temporally linked to the expression of CSF1R, CD36, MSR1 and SCARB1; 7 miRNAs linked to the regulation of the transcription factors RUNX1 and PU.1, and 14 miRNAs target the nuclear receptor PPARa and PPAR¿. This novel information provides an important reference resource for further study of the functional links between miRNAs and their target mRNAs for the regulation of differentiation and function of macrophages.

DOI 10.18632/oncotarget.8933
Citations Scopus - 5Web of Science - 6
Co-authors Hock Tay, Paul Foster
2016 Thi HN, Maltby S, Eyers F, Foster PS, Yang M, 'Bromodomain and Extra Terminal (BET) Inhibitor Suppresses Macrophage-Driven Steroid-Resistant Exacerbations of Airway Hyper-Responsiveness and Inflammation', PLOS ONE, 11 (2016) [C1]
DOI 10.1371/journal.pone.0163392
Citations Scopus - 12Web of Science - 11
Co-authors Steven Maltby, Paul Foster
2015 Tay HL, Kaiko GE, Plank M, Li J, Maltby S, Essilfie A-T, et al., 'Correction: Antagonism of miR-328 Increases the Antimicrobial Function of Macrophages and Neutrophils and Rapid Clearance of Non-typeable Haemophilus Influenzae (NTHi) from Infected Lung.', PLoS pathogens, 11 e1004956 (2015) [O1]
DOI 10.1371/journal.ppat.1004956
Citations Scopus - 2
Co-authors Steven Maltby, Hock Tay, Philip Hansbro, Gerard Kaiko, Paul Foster, Joerg Mattes
2015 Li JJ, Tay HL, Maltby S, Xiang Y, Eyers F, Hatchwell L, et al., 'MicroRNA-9 regulates steroid-resistant airway hyperresponsiveness by reducing protein phosphatase 2A activity', Journal of Allergy and Clinical Immunology, 136 462-473 (2015) [C1]

Background Steroid-resistant asthma is a major clinical problem that is linked to activation of innate immune cells. Levels of IFN-¿ and LPS are often increased in these patients.... [more]

Background Steroid-resistant asthma is a major clinical problem that is linked to activation of innate immune cells. Levels of IFN-¿ and LPS are often increased in these patients. Cooperative signaling between IFN-¿/LPS induces macrophage-dependent steroid-resistant airway hyperresponsiveness (AHR) in mouse models. MicroRNAs (miRs) are small noncoding RNAs that regulate the function of innate immune cells by controlling mRNA stability and translation. Their role in regulating glucocorticoid responsiveness and AHR remains unexplored. Objective IFN-¿ and LPS synergistically increase the expression of miR-9 in macrophages and lung tissue, suggesting a role in the mechanisms of steroid resistance. Here we demonstrate the role of miR-9 in IFN-¿/LPS-induced inhibition of dexamethasone (DEX) signaling in macrophages and in induction of steroid-resistant AHR. Methods MiRNA-9 expression was assessed by means of quantitative RT-PCR. Putative miR-9 targets were determined in silico and confirmed in luciferase reporter assays. miR-9 function was inhibited with sequence-specific antagomirs. The efficacy of DEX was assessed by quantifying glucocorticoid receptor (GR) cellular localization, protein phosphatase 2A (PP2A) activity, and AHR. Results Exposure of pulmonary macrophages to IFN-¿/LPS synergistically induced miR-9 expression; reduced levels of its target transcript, protein phosphatase 2 regulatory subunit B (B56) d isoform; attenuated PP2A activity; and inhibited DEX-induced GR nuclear translocation. Inhibition of miR-9 increased both PP2A activity and GR nuclear translocation in macrophages and restored steroid sensitivity in multiple models of steroid-resistant AHR. Pharmacologic activation of PP2A restored DEX efficacy and inhibited AHR. MiR-9 expression was increased in sputum of patients with neutrophilic but not those with eosinophilic asthma. Conclusion MiR-9 regulates GR signaling and steroid-resistant AHR. Targeting miR-9 function might be a novel approach for the treatment of steroid-resistant asthma.

DOI 10.1016/j.jaci.2014.11.044
Citations Scopus - 57Web of Science - 55
Co-authors Joerg Mattes, Paul Foster, Steven Maltby, Hock Tay
2015 Tay HL, Kaiko GE, Plank M, Li JJ, Maltby S, Essilfie AT, et al., 'Antagonism of miR-328 Increases the Antimicrobial Function of Macrophages and Neutrophils and Rapid Clearance of Non-typeable Haemophilus Influenzae (NTHi) from Infected Lung', PLoS Pathogens, 11 (2015) [C1]

Pathogenic bacterial infections of the lung are life threatening and underpin chronic lung diseases. Current treatments are often ineffective potentially due to increasing antibio... [more]

Pathogenic bacterial infections of the lung are life threatening and underpin chronic lung diseases. Current treatments are often ineffective potentially due to increasing antibiotic resistance and impairment of innate immunity by disease processes and steroid therapy. Manipulation miRNA directly regulating anti-microbial machinery of the innate immune system may boost host defence responses. Here we demonstrate that miR-328 is a key element of the host response to pulmonary infection with non-typeable haemophilus influenzae and pharmacological inhibition in mouse and human macrophages augments phagocytosis, the production of reactive oxygen species, and microbicidal activity. Moreover, inhibition of miR-328 in respiratory models of infection, steroid-induced immunosuppression, and smoke-induced emphysema enhances bacterial clearance. Thus, miRNA pathways can be targeted in the lung to enhance host defence against a clinically relevant microbial infection and offer a potential new anti-microbial approach for the treatment of respiratory diseases.

DOI 10.1371/journal.ppat.1004549
Citations Scopus - 44Web of Science - 49
Co-authors Paul Foster, Steven Maltby, Hock Tay, Philip Hansbro, Joerg Mattes, Gerard Kaiko
2014 Yang M, Eyers F, Xiang Y, Guo M, Young IG, Rosenberg HF, Foster PS, 'Expression profiling of differentiating eosinophils in bone marrow cultures predicts functional links between microRNAs and their target mRNAs', PLoS ONE, 9 (2014) [C1]

Background: MicroRNAs (miRNAs) are small non-coding RNAs that regulate complex transcriptional networks underpin immune responses. However, little is known about the specific miRN... [more]

Background: MicroRNAs (miRNAs) are small non-coding RNAs that regulate complex transcriptional networks underpin immune responses. However, little is known about the specific miRNA networks that control differentiation of specific leukocyte subsets. In this study, we profiled miRNA expression during differentiation of eosinophils from bone marrow (BM) progenitors (bmEos), and correlated expression with potential mRNA targets involved in crucial regulatory functions. Profiling was performed on whole BM cultures to document the dynamic changes in miRNA expression in the BM microenvironment over the differentiation period. miRNA for network analysis were identified in BM cultures enriched in differentiating eosinophils, and chosen for their potential ability to target mRNA of factors that are known to play critical roles in eosinophil differentiation pathways or cell identify. Methodology/Principal Findings: We identified 68 miRNAs with expression patterns that were up- or down- regulated 5-fold or more during bmEos differentiation. By employing TargetScan and MeSH databases, we identified 348 transcripts involved in 30 canonical pathways as potentially regulated by these miRNAs. Furthermore, by applying miRanda and Ingenuity Pathways Analysis (IPA), we identified 13 specific miRNAs that are temporally associated with the expression of IL-5Ra and CCR3 and 14 miRNAs associated with the transcription factors GATA-1/2, PU.1 and C/EBPe. We have also identified 17 miRNAs that may regulate the expression of TLRs 4 and 13 during eosinophil differentiation, although we could identify no miRNAs targeting the prominent secretory effector, eosinophil major basic protein. Conclusions/Significance: This is the first study to map changes in miRNA expression in whole BM cultures during the differentiation of eosinophils, and to predict functional links between miRNAs and their target mRNAs for the regulation of eosinophilopoiesis. Our findings provide an important resource that will promote the platform for further understanding of the role of these non-coding RNAs in the regulation of eosinophil differentiation and function. © 2014 Yang et al.

DOI 10.1371/journal.pone.0097537
Citations Scopus - 15Web of Science - 14
Co-authors Paul Foster
2014 Xiang Y, Eyers F, Young IG, Rosenberg HF, Foster PS, Yang M, 'Identification of MicroRNAs regulating the developmental pathways of bone marrow derived mast cells', PLoS ONE, 9 (2014) [C1]

Background: MicroRNAs (miRNAs) play important roles in leukocyte differentiation, although those utilised for specific programs and key functions remain incompletely characterised... [more]

Background: MicroRNAs (miRNAs) play important roles in leukocyte differentiation, although those utilised for specific programs and key functions remain incompletely characterised. As a global approach to gain insights into the potential regulatory role of miRNA in mast cell differentiation we characterised expression in BM cultures from the initiation of differentiation. In cultures enriched in differentiating mast cells we characterised miRNA expression and identified miRNA targeting the mRNA of putative factors involved in differentiation pathways and cellular identity. Detailed pathway analysis identified a unique miRNA network that is intimately linked to the mast cell differentiation program. Methodology/Principal Findings: We identified 86 unique miRNAs with expression patterns that were up- or down-regulated at 5-fold or more during bone marrow derived mast cells (BMMC) development. By employing TargetScan and MeSH databases, we identified 524 transcripts involved in 30 canonical pathways as potentially regulated by these specific 86 miRNAs. Furthermore, by applying miRanda and IPA analyses, we predict that 7 specific miRNAs of this group are directly associated with the expression of c-Kit and FceRIa and likewise, that 18 miRNAs promote expression of Mitf, GATA1 and c/EBPa three core transcription factors that direct mast cell differentiation. Furthermore, we have identified 11 miRNAs that may regulate the expression of STATs-3, -5a/b, GATA2 and GATA3 during differentiation, along with 13 miRNAs that target transcripts encoding Ndst2, mMCP4 and mMCP6 and thus may regulate biosynthesis of mast cell secretory mediators. Conclusions/ Significance: This investigation characterises changes in miRNA expression in whole BM cultures during the differentiation of mast cells and predicts functional links between miRNAs and their target mRNAs for the regulation of development. This information provides an important resource for further investigations of the contributions of miRNAs to mast cell differentiation and function. © 2014 Xiang et al.

DOI 10.1371/journal.pone.0098139
Citations Scopus - 16Web of Science - 12
Co-authors Paul Foster
2013 Eftekhari P, Hajizadeh S, Reza Raoufy M, Reza Masjedi M, Yang M, Hansbro N, et al., 'Preventive effect of N-acetylcysteine in a mouse model of steroid resistant acute exacerbation of asthma', EXCLI Journal, 12 184-192 (2013) [C1]

Oxidative stress appears to have an important role in glucocorticoid insensitivity, as a crucial problem in asthma therapy. We studied the preventive effect of antioxidant N-acety... [more]

Oxidative stress appears to have an important role in glucocorticoid insensitivity, as a crucial problem in asthma therapy. We studied the preventive effect of antioxidant N-acetylcysteine (NAC) on the airway hyper-responsiveness (AHR) and the accumulation of inflammatory cells in the airways in an animal model of steroid resistant acute exacerbation of asthma. Systemically sensitized Balb/C mice were exposed to Ovalbumin aerosol on days 13, 14, 15 and 16, followed by intratracheal lipopolysaccharide (LPS) to induce acute exacerbation. NAC (intraperitoneal, 320 mg/kg 30 min before and 12 hours after each challenge) reduced hyperresponsiveness with/out dexamethasone. LPS application caused neutrophilia in bronchoalveolar lavage fluid (BALF) and eosinophil count was higher than respective control in BALF as well as neutrophils after dexamethasone treatment. NAC significantly decreased neutrophil and eosinophil count in BALF as well as inflammatory cytokines (IL-13 and IL-5).We concluded that addition of NAC to asthma therapy has beneficial preventive effects in an animal model of steroid resistant acute exacerbation of asthma.

Citations Scopus - 15Web of Science - 13
Co-authors Paul Foster
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]
Citations Scopus - 145Web of Science - 144
Co-authors Peter Wark, Emma Beckett, Jay Horvat, Philip Hansbro, Simon Keely, Paul Foster
2013 Foster PS, Plank MW, Collison AM, Tay HL, Kaiko GE, Li J, et al., 'The emerging role of microRNAs in regulating immune and inflammatory responses in the lung', Immunological Reviews, 253 198-215 (2013) [C1]
Citations Scopus - 75Web of Science - 75
Co-authors Gerard Kaiko, Adam Collison, Philip Hansbro, Hock Tay, Paul Foster, Joerg Mattes
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]
Citations Scopus - 64Web of Science - 65
Co-authors Gerard Kaiko, Jay Horvat, Paul Foster, Philip Hansbro, Malcolm Starkey
2013 Li JJ, Tay HL, Plank M, Essilfie A-T, Hansbro PM, Foster PS, Yang M, 'Activation of Olfactory Receptors on Mouse Pulmonary Macrophages Promotes Monocyte Chemotactic Protein-1 Production', PLOS ONE, 8 (2013) [C1]
DOI 10.1371/journal.pone.0080148
Citations Scopus - 26Web of Science - 11
Co-authors Philip Hansbro, Hock Tay, Paul Foster
2012 Yang M, Kumar RK, Hansbro PM, Foster PS, 'Emerging roles of pulmonary macrophages in driving the development of severe asthma', Journal of Leukocyte Biology, 91 557-569 (2012) [C1]
Citations Scopus - 69Web of Science - 70
Co-authors Philip Hansbro, Paul Foster
2012 Kumar RK, Yang M, Herbert C, Foster PS, 'Interferon- , pulmonary macrophages and airway responsiveness in asthma', Inflammation and Allergy - Drug Targets, 11 292-297 (2012) [C1]
Citations Scopus - 22
Co-authors Paul Foster
2011 Wang W, Hansbro PM, Foster PS, Yang M, 'An alternate STAT6-independent pathway promotes eosinophil influx into blood during allergic airway inflammation', PLoS ONE, 6 (2011) [C1]
DOI 10.1371/journal.pone.0017766
Citations Scopus - 9Web of Science - 7
Co-authors Paul Foster, Philip Hansbro
2010 Li J, Wang W, Baines KJ, Bowden NA, Hansbro PM, Gibson PG, et al., 'IL-27/IFN-y induce MyD88-dependent steroid-resistant airway hyperresponsiveness by inhibiting glucocorticoid signaling in macrophages', Journal of Immunology, 185 4401-4409 (2010) [C1]
DOI 10.4049/jimmunol.1001039
Citations Scopus - 85Web of Science - 81
Co-authors Nikola Bowden, Katherine Baines, Philip Hansbro, Peter Gibson, Paul Foster
2010 Yang M, Kumar RK, Foster PS, 'Interferon-Y and pulmonary macrophages contribute to the mechanisms underlying prolonged airway hyperresponsiveness', Clinical and Experimental Allergy, 40 163-173 (2010) [C1]
DOI 10.1111/j.1365-2222.2009.03393.x
Citations Scopus - 34Web of Science - 31
Co-authors Paul Foster
2010 Hardy CL, Lemasurier JS, Olsson F, Dang T, Yao J, Yang M, et al., 'Interleukin-13 regulates secretion of the tumor growth factor-beta superfamily cytokine activin A in allergic airway inflammation', American Journal of Respiratory Cell and Molecular Biology, 42 667-675 (2010) [C1]
DOI 10.1165/rcmb.2008-0429OC
Citations Scopus - 22Web of Science - 21
2010 Wang W, Li J, Foster PS, Hansbro PM, Yang M, 'Potential therapeutic targets for steroid-resistant asthma', Current Drug Targets, 11 957-970 (2010) [C1]
DOI 10.2174/138945010791591412
Citations Scopus - 55Web of Science - 60
Co-authors Philip Hansbro, Paul Foster
2009 Yang M, Kumar RK, Foster PS, 'Pathogenesis of steroid-resistant airway hyperresponsiveness: Interaction between IFN-gamma and TLR4/MyD88 pathways', Journal of Immunology, 182 5107-5115 (2009) [C1]
DOI 10.4049/jimmunol.0803468
Citations Scopus - 67Web of Science - 59
Co-authors Paul Foster
2008 Yang M, Mattes J, 'Discovery, biology and therapeutic potential of RNA interference, microRNA and antagomirs', Pharmacology & Therapeutics, 117 94-104 (2008) [C1]
DOI 10.1016/j.pharmthera.2007.08.004
Citations Scopus - 79Web of Science - 73
Co-authors Joerg Mattes
2007 Mattes J, Yang M, Foster PS, 'Regulation of microRNA by antagomirs: a new class of pharmacological antagonists for the specific regulation of gene function?', American Journal of Respiratory and Cellular Molecular Biology, 36 8-12 (2007) [C1]
DOI 10.1165/rcmb.2006-0227TR
Citations Scopus - 67Web of Science - 62
Co-authors Paul Foster, Joerg Mattes
2007 Webb DC, Yang M, Matthaei (Ext) K, Foster PS, 'Comparative roles of IL-4, IL-13, and IL-4Ralpha in dendritic cell maturation and CD4+ Th2 cell function', Journal of Immunology, 178 219-227 (2007) [C1]
Citations Scopus - 61Web of Science - 59
Co-authors Paul Foster
2006 Yang M, Rangasamy D, Matthaei KI, Frew AJ, Zimmmermann N, Mahalingam S, et al., 'Inhibition of arginase I activity by RNA interference attenuates IL-13-induced airways hyperresponsiveness', Journal of Immunology, 177 5595-5603 (2006) [C1]
DOI 10.4049/jimmunol.177.8.5595
Citations Scopus - 87Web of Science - 80
Co-authors Paul Foster
2006 Yang M, Mattes J, Hansbro PM, Foster PS, 'Employment of microRNA profiles and RNA interference and antagomirs for the characterization and treatment of respiratory disease', Drug Discovery Today: Therapeutic Strategies, 3 325-332 (2006) [C1]
DOI 10.1016/j.ddstr.2006.10.001
Citations Scopus - 5
Co-authors Philip Hansbro, Paul Foster, Joerg Mattes
2006 Yang M, Rangasamy D, Matthaei K, Frew A, Zimmmermann N, Mahalingham S, et al., 'Inhibition of arginase I activity by RNA interference attenuates interleukin-13 induced airways hyperresponsiveness', ACTA PHARMACOLOGICA SINICA, 27 266-266 (2006)
Co-authors Paul Foster
2006 Siegle JS, Hansbro NG, Herbert C, Yang M, Foster PS, Kumar RK, 'Airway hyperreactivity in exacerbation of chronic asthma is independent of elosinophilic inflammation', American Journal of Respiratory Cell and Molecular Biology, 35 565-570 (2006) [C1]
DOI 10.1165/rcmb.2006-0135OC
Citations Scopus - 48Web of Science - 45
Co-authors Paul Foster
2004 Forbes E, Smart V, D'Aprile A, Henry P, Yang M, Matthaei KI, et al., 'T Helper-2 Immunity Regulates Bronchial Hyperresponsiveness in Eosinophil-Associated Gastrointestinal Disease in Mice', Gastroenterology, 127 105-118 (2004) [C1]
DOI 10.1053/j.gastro.2004.03.057
Citations Scopus - 22Web of Science - 20
Co-authors Paul Foster
2004 Forbes E, Murase T, Yang M, Matthaei KI, Lee JJ, Lee NA, et al., 'Immunopathogenesis of experimental ulcerative colitis is mediated by eosinophil peroxidase1', J Immunol, 172 5664-5675 (2004) [C1]
Citations Scopus - 130Web of Science - 114
Co-authors Paul Foster
2004 Fulkerson PC, Zimmermann N, Brandt EB, Muntel EE, Doepker MP, Kavanaugh JL, et al., 'Negative regulation of eosinophil recruitment to the lung by the chemokine monokine induced by INF-g (Mig, CXCL9)', Proceedings of the National Academy of Sciences of the USA, 101 1987-1992 (2004) [C1]
DOI 10.1073/pnas.0308544100
Citations Scopus - 85Web of Science - 82
Co-authors Paul Foster
2003 Foster PS, Yang M, Mattes J, Kumar R, Webb D, 'Interleukin-13 and allergy', Modern Aspects of Immunobiology, 3 8 (2003)
Co-authors Paul Foster, Joerg Mattes
2003 Zimmerman N, King NE, Laporte J, Yang M, Mishra A, Pope S, et al., 'Dissection of experimental asthma with DNA microarray analysis identifies arginase in asthma pathogenesis', Journal of Clinical Investigation, 111 1863-1874 (2003) [C1]
DOI 10.1172/JCI200317912
Citations Scopus - 428Web of Science - 402
Co-authors Paul Foster
2003 Kumar RK, Herbert C, Thomas PS, Wollin L, Beume R, Yang M, et al., 'Inhibition of inflammation and remodeling by roflumilast and dexamethasone in murine chronic asthma', Journal of Pharmacology and Experimental Therapeutics, 307 349-355 (2003) [C1]
DOI 10.1124/jpet.103.053819
Citations Scopus - 144Web of Science - 121
Co-authors Paul Foster
2003 Yang M, Hogan SP, Mahalingam S, Pope SM, Zimmerman N, Fulkerson P, et al., 'Eotaxin-2 and IL-5 cooperate in the lung to regulate IL-13 production and airway eosinophilia and hyperreactivity', Journal of Allergy and Clinical Immunology, 112 935-943 (2003) [C1]
DOI 10.1016/j.jaci.2003.08.010
Citations Scopus - 98
Co-authors Paul Foster
2003 Foster PS, Webb DC, Yang M, Herbert C, Kumar RK, 'Dissociation of T helper type 2 cytokine-dependent airway lesions from signal transducer and activator of transcription 6 signalling in experimental chronic asthma', Clinical and Experimental Allergy, 33 688-695 (2003) [C1]
DOI 10.1046/j.1365-2222.2003.01647.x
Citations Scopus - 47Web of Science - 44
Co-authors Paul Foster
2002 Mattes J, Yang M, Mahalinggam S, Kuehr J, Webb DC, Simson L, et al., 'Intrinsic defect in T cell production of interleukin (IL)-13 in the absence of both IL-5 and cotaxin precludes the development of eosinophilia and airways hyperreactivity in experimental asthma.', J Exp Med. 195:1433-44, 1433-1444 (2002) [C1]
Citations Scopus - 227Web of Science - 213
Co-authors Paul Foster, Joerg Mattes
2002 Foster PS, Yang M, Herbert C, Kumar R, 'CD4+ T-lymphocytes regulate airway remodeling and hyper-reactivity in a mouse model of chronic asthma', Laboratory Investigation, 82 455-462 (2002) [C1]
Citations Web of Science - 47
Co-authors Paul Foster
2002 Foster PS, Hogan S, Yang M, Mattes J, Young I, Matthaei K, et al., 'Interleukin-5 and eosinophils as therapeutic targets for asthma', Trends in Molecular Medicine, 8 162-167 (2002) [C2]
Citations Scopus - 64Web of Science - 57
Co-authors Paul Foster, Joerg Mattes
2002 Kumar R, Herbert C, Yang M, Koskinen A, McKenzie A, Foster PS, 'Role of interleukin-13 in eosinophil accumulation and airway remodelling in a mouse model of chronic asthma', Clinical and Experimental Allergy, 32 1104-1111 (2002) [C1]
Citations Scopus - 157Web of Science - 126
Co-authors Paul Foster
2002 Foster PS, Yang M, Herbert C, Kumar RK, 'CD4

Asthma is an acute-on-chronic inflammatory disease of the airways, characterized by airflow obstruction and hyper-reactivity of the airways to a variety of stimuli. Chronic asthma... [more]

Asthma is an acute-on-chronic inflammatory disease of the airways, characterized by airflow obstruction and hyper-reactivity of the airways to a variety of stimuli. Chronic asthma is associated with remodeling of the airway wall, which may contribute to hyper-reactivity and fixed airflow obstruction. We used an improved mouse model of chronic asthma to investigate the role of CD4+ T-lymphocytes in airway remodeling and hyper-reactivity. Animals functionally depleted of CD4+ T-lymphocytes by repeated administration of a monoclonal antibody exhibited markedly decreased airway responsiveness. In addition, these mice had greatly diminished subepithelial fibrosis, epithelial thickening, and mucous cell hyperplasia/metaplasia. Chronic inflammation in the airway wall was moderately reduced, with a marked decrease in the accumulation of immunoglobulin- synthesizing plasma cells. However, intraepithelial accumulation of eosinophils was not significantly inhibited and airway epithelial expression of eotaxin was undiminished. This work provides the first experimental evidence that CD4+ T-lymphocytes play a crucial role in the pathogenesis of the lesions of chronic asthma and lends support to the notion that functional inhibition of these cells may be an important therapeutic target.

DOI 10.1038/labinvest.3780438
Citations Scopus - 52
Co-authors Paul Foster
2002 Yang M, Hogan SP, Henry P, Matthaei KI, McKenzie ANJ, Young IG, et al., 'Interleukin-(IL)-13 mediates biphasic airways hyperreactivity through the IL-4 receptor-alpha chain and STAT-6 independently of IL-5 and eotaxin', JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 109 S360-S360 (2002)
DOI 10.1016/S0091-6749(02)82255-2
Co-authors Paul Foster
2001 Mattes J, Yang M, Siqueira A, Clark K, Mackenzie J, McKenzie A, et al., 'IL-13 induces airways hyperreactivity independently of the IL-4R{alpha} chain in the allergic lung', Journal of Immunology, 167 1683-1692 (2001) [C1]
Citations Scopus - 130Web of Science - 121
Co-authors Paul Foster, Joerg Mattes
2001 Foster PS, Mould A, Yang M, Mackenzie J, Mattes J, Hogan S, et al., 'Elemental signals regulating eosinophil accumulation in the lung', Immunological Reviews, 179 173-181 (2001) [C2]
Citations Scopus - 199Web of Science - 176
Co-authors Joerg Mattes, Paul Foster
2001 Yang M, Hogan S, Henry P, Matthaei K, McKenzie A, Young I, et al., 'Interleukin-13 mediates airways hyperreactivity through the IL-4 receptor-alpha chain and STAT-6 independently of IL-5 and eotaxin', American Journal of Respiratory Cell and Molecular Biology, 25 522-530 (2001) [C1]
Citations Scopus - 134Web of Science - 123
Co-authors Paul Foster
2000 Webb D, McKenzie A, Koskinen A, Yang M, Mattes J, Foster PS, 'Integrated signals between IL-13, IL-4, and IL-5 regulate airways hyperreactivity', Journal of Immunology, 165 108-113 (2000) [C1]
Citations Scopus - 275Web of Science - 253
Co-authors Paul Foster, Joerg Mattes
2000 Foster PS, Ming Y, Matthei K, Young I, Temelkovski J, Kumar R, 'Dissociation of inflammatory and epithelial responses in a murine model of chronic asthma', Laboratory Investigation, 80 655-662 (2000) [C1]
Citations Scopus - 85Web of Science - 78
Co-authors Paul Foster
Show 63 more journal articles

Review (2 outputs)

Year Citation Altmetrics Link
2017 Foster PS, Maltby S, Rosenberg HF, Tay HL, Hogan SP, Collison AM, et al., 'Modeling T

In this review, we highlight experiments conducted in our laboratories that have elucidated functional roles for CD4+ T-helper type-2 lymphocytes (TH2 cells), their associated cyt... [more]

In this review, we highlight experiments conducted in our laboratories that have elucidated functional roles for CD4+ T-helper type-2 lymphocytes (TH2 cells), their associated cytokines, and eosinophils in the regulation of hallmark features of allergic asthma. Notably, we consider the complexity of type-2 responses and studies that have explored integrated signaling among classical TH2 cytokines (IL-4, IL-5, and IL-13), which together with CCL11 (eotaxin-1) regulate critical aspects of eosinophil recruitment, allergic inflammation, and airway hyper-responsiveness (AHR). Among our most important findings, we have provided evidence that the initiation of TH2 responses is regulated by airway epithelial cell-derived factors, including TRAIL and MID1, which promote TH2 cell development via STAT6-dependent pathways. Further, we highlight studies demonstrating that microRNAs are key regulators of allergic inflammation and potential targets for anti-inflammatory therapy. On the background of TH2 inflammation, we have demonstrated that innate immune cells (notably, airway macrophages) play essential roles in the generation of steroid-resistant inflammation and AHR secondary to allergen- and pathogen-induced exacerbations. Our work clearly indicates that understanding the diversity and spatiotemporal role of the inflammatory response and its interactions with resident airway cells is critical to advancing knowledge on asthma pathogenesis and the development of new therapeutic approaches.

DOI 10.1111/imr.12549
Citations Scopus - 58Web of Science - 55
Co-authors Steven Maltby, Paul Foster, Joerg Mattes, Gerard Kaiko, Adam Collison, Philip Hansbro, Hock Tay
2017 Maltby S, Tay HL, Yang M, Foster PS, 'Mouse models of severe asthma: Understanding the mechanisms of steroid resistance, tissue remodelling and disease exacerbation', Respirology (2017) [C1]

Severe asthma has significant disease burden and results in high healthcare costs. While existing therapies are effective for the majority of asthma patients, treatments for indiv... [more]

Severe asthma has significant disease burden and results in high healthcare costs. While existing therapies are effective for the majority of asthma patients, treatments for individuals with severe asthma are often ineffective. Mouse models are useful to identify mechanisms underlying disease pathogenesis and for the preclinical assessment of new therapies. In fact, existing mouse models have contributed significantly to our understanding of allergic/eosinophilic phenotypes of asthma and facilitated the development of novel targeted therapies (e.g. anti-IL-5 and anti-IgE). These therapies are effective in relevant subsets of severe asthma patients. Unfortunately, non-allergic/non-eosinophilic asthma, steroid resistance and disease exacerbation remain areas of unmet clinical need. No mouse model encompasses all features of severe asthma. However, mouse models can provide insight into pathogenic pathways that are relevant to severe asthma. In this review, as examples, we highlight models relevant to understanding steroid resistance, chronic tissue remodelling and disease exacerbation. Although these models highlight the complexity of the immune pathways that may underlie severe asthma, they also provide insight into new potential therapeutic approaches.

DOI 10.1111/resp.13052
Citations Scopus - 32Web of Science - 30
Co-authors Hock Tay, Paul Foster, Steven Maltby

Conference (14 outputs)

Year Citation Altmetrics Link
2019 Thi HN, Eyers F, Yang M, Foster P, 'LSC-2019-Azithromycin modulates viral-induced asthma exacerbation by targeting the innate immune response', EUROPEAN RESPIRATORY JOURNAL, Madrid, SPAIN (2019)
DOI 10.1183/13993003.congress-2019.OA1623
Co-authors Paul Foster
2017 Simpson JL, Pabreja K, Baines KJ, Eyres F, Yang M, Nair P, et al., 'Sputum Il-27 Gene Expression In Asthma Endotypes', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Washington, DC (2017)
Co-authors Peter Gibson, Katherine Baines, Paul Foster, Jodie Simpson
2017 Tay HL, Hsu A, Nguyen T, Donovan C, Collison A, Mattes J, et al., 'Interleukin-36 gamma: Roles in lungs innate immunity, inflammation and allergy', CYTOKINE, Int Cytokine & Interferon Soc, Kanazawa, JAPAN (2017)
Co-authors Paul Foster, Chantal Donovan, Joerg Mattes, Hock Tay, Philip Hansbro, Gerard Kaiko, Alan Hsu, Adam Collison
2017 Pabreja K, Gibson PG, Baines KJ, Eyers F, Yang M, Nair P, et al., 'INCREASED EXPRESSION OF IL-27 IN NEUTROPHILIC ASTHMA', RESPIROLOGY (2017)
Co-authors Katherine Baines, Paul Foster, Jodie Simpson, Peter Gibson
2017 Nguyen TH, Maltby S, Simpson JL, Eyers F, Baines KJ, Gibson PG, et al., 'MACROPHAGES REGULATE THE DEVELOPMENT OF RSV INDUCED ASTHMA EXACERBATIONS', RESPIROLOGY (2017)
Co-authors Katherine Baines, Peter Gibson, Jodie Simpson, Steven Maltby, Paul Foster
2017 Pabreja K, Gibson P, Baines K, Eyers F, Yang M, Nair P, et al., 'IL-27 and asthma endotypes-Is there a connection', EUROPEAN RESPIRATORY JOURNAL, Milan, ITALY (2017)
DOI 10.1183/1393003.congress-2017.PA1159
Citations Web of Science - 1
Co-authors Katherine Baines, Peter Gibson, Paul Foster
2016 Hadjigol S, Maltby S, Yang M, Foster P, 'UNDERSTANDING MECHANISMS OF BACTERIAL-INDUCED DISEASE EXACERBATION IN A MOUSE MODEL OF ALLERGIC AIRWAYS DISEASE', RESPIROLOGY (2016)
Co-authors Steven Maltby, Paul Foster
2016 Tay H, Yang M, Hsu A, Nguyen T-H, Plank M, Maltby S, et al., 'Role of interleukin-36 gamma in regulating lung inflammation', EUROPEAN JOURNAL OF IMMUNOLOGY, Melbourne, AUSTRALIA (2016)
Co-authors Paul Foster, Philip Hansbro, Alan Hsu, Nathan Bartlett, Steven Maltby
2016 Nguyen TH, Maltby S, Simpson JL, Eyers F, Gibson PG, Foster PS, Yang M, 'Macrophages regulate steroid resistant airway inflammation in a mouse model of respiratory syncytial virus-induced asthma exacerbation', EUROPEAN JOURNAL OF IMMUNOLOGY, Melbourne, AUSTRALIA (2016)
Co-authors Paul Foster, Jodie Simpson, Steven Maltby, Peter Gibson
2015 Tay H, Kaiko G, Plank M, Li J, Essilfie A, Maltby S, et al., 'THE ROLE OF MIR-328 IN RESPIRATORY DISEASES', RESPIROLOGY, Queensland, AUSTRALIA (2015) [E3]
Co-authors Paul Foster, Steven Maltby, Philip Hansbro, Gerard Kaiko, Joerg Mattes, Hock Tay
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]
Co-authors Paul Foster, Philip Hansbro, Simon Keely, Emma Beckett, Peter Wark, Jay Horvat
2012 Li J, Foster PS, Yang M, 'Inducible microRNA-X expression underpins steroid- resistant airway hyperresponsiveness by upregulating IL-27 expression', Respirology, Canberra, ACT (2012) [E3]
Citations Web of Science - 1
Co-authors Paul Foster
2011 Foster P, Li J, Wang W, Baines K, Bowden N, Hansbro P, et al., 'IL-27 underpins steroid resistant airway hyperresponsiveness via MyD88 dependent pathways', ALLERGY, Istanbul, TURKEY (2011) [E3]
Co-authors Philip Hansbro, Nikola Bowden, Peter Gibson, Paul Foster
2008 Yang M, Ma C, Foster PS, 'Antigen-specific TH1 cells induce airway hyper-reactivity in co-operation with lipopolysaccharide in BALB/C mice', Respirology, Melbourne, VIC (2008) [E3]
DOI 10.1111/j.1440-1843.2008.01252.x
Co-authors Paul Foster
Show 11 more conferences
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Grants and Funding

Summary

Number of grants 22
Total funding $6,775,290

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


20191 grants / $1,318,180

Modelling the role of innate immune cells in exacerbation of asthma$1,318,180

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Doctor Hock Tay, Doctor Ming Yang, Doctor Ming Yang
Scheme Project Grant
Role Investigator
Funding Start 2019
Funding Finish 2023
GNo G1800443
Type Of Funding C1100 - Aust Competitive - NHMRC
Category 1100
UON Y

20171 grants / $844,726

Shared innate immune mechanisms underpin-steroid resistant pathogen-induced asthma exacerbations$844,726

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Doctor Ming Yang, Associate Professor Nathan Bartlett
Scheme Project Grant
Role Investigator
Funding Start 2017
Funding Finish 2020
GNo G1600084
Type Of Funding C1100 - Aust Competitive - NHMRC
Category 1100
UON Y

20152 grants / $22,000

Blocking the negative effects of stress on the brain to promote better healing of the brain after stroke$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Rohan Walker, Doctor Lin Kooi Ong, Doctor Ming Yang, Professor Sarah Johnson
Scheme Project Grant
Role Investigator
Funding Start 2015
Funding Finish 2015
GNo G1501384
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

9th Biennial Symposium of the International Esoinophil Society, Chicago USA, 14-18 July 2015$2,000

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

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Ming Yang
Scheme Travel Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1500734
Type Of Funding Internal
Category INTE
UON Y

20141 grants / $700,623

New way of treating respiratory infections and airway inflammatory diseases by targeting miRNA $700,623

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Doctor Ming Yang
Scheme Project Grant
Role Investigator
Funding Start 2014
Funding Finish 2016
GNo G1300121
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

20131 grants / $20,000

DP73 Digital colour and monochrome camera + cellSens software + Xcite120 fluorescence lamp illuminator$20,000

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Doctor Alan Hsu, Professor Phil Hansbro, Professor Joerg Mattes, Doctor Katie Baines, Professor Jodie Simpson, Professor Rakesh Kumar, Doctor Nicole Hansbro, Doctor Steven Maltby, Doctor Ming Yang, Doctor Gerard Kaiko, Associate 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

20122 grants / $564,551

Understanding the mechanisms of steroid resistant inflammatory pathways in mouse models of asthma: potential new treatment approaches$514,551

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Doctor Ming Yang
Scheme Project Grant
Role Investigator
Funding Start 2012
Funding Finish 2014
GNo G1100099
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

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 Laureate Professor Paul Foster, Professor Phil Hansbro, Professor Joerg Mattes, Professor Rakesh Kumar, Doctor Nicole Hansbro, Doctor Ming Yang, Associate Professor Jay Horvat, Professor Simon Keely, Doctor Andrew Jarnicki, Doctor Linda Howland, Doctor 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

20113 grants / $429,250

Targeting pro-survival mechanisms to sensitize human melanoma to immunotherapy$359,250

Funding body: Cancer Council NSW

Funding body Cancer Council NSW
Project Team Professor Xu Dong Zhang, Doctor Ming Yang
Scheme Research Program
Role Investigator
Funding Start 2011
Funding Finish 2013
GNo G1000379
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

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, Laureate Professor Paul Foster, Professor Joerg Mattes, Professor Simon Keely, Associate Professor Jay Horvat, Doctor Nicole Hansbro, Doctor Ming Yang, Doctor Catherine Ptaschinski, Doctor Kelly Asquith, Doctor Gough Au, Conjoint Professor Peter Wark, Laureate 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

Targeting Pro-Survival Mechanisms to Sensitize Human Melanoma to Immunotherapy$25,000

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Professor Xu Dong Zhang, Doctor Ming Yang
Scheme Near Miss Grant
Role Investigator
Funding Start 2011
Funding Finish 2011
GNo G1001046
Type Of Funding Internal
Category INTE
UON Y

20102 grants / $40,509

Buxco FinePointe software and FinePointe RC system for mice $39,000

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Professor Phil Hansbro, Professor Joerg Mattes, Doctor Nicole Hansbro, Doctor Simon Phipps, Doctor Ming Yang, Doctor Kelly Asquith, Doctor Catherine Ptaschinski, Professor Rakesh Kumar, Professor Judith Black
Scheme Equipment Grant
Role Investigator
Funding Start 2010
Funding Finish 2010
GNo G1000053
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

40th Annual Scientific Meting for Australiasian Society for Immunology 2010, Perth, 5 - 9 December 2010$1,509

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

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Ming Yang
Scheme Travel Grant
Role Lead
Funding Start 2010
Funding Finish 2011
GNo G1001004
Type Of Funding Internal
Category INTE
UON Y

20091 grants / $41,150

Coulter counter$41,150

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Professor Phil Hansbro, Professor Joerg Mattes, Doctor Simon Phipps, Doctor Ming Yang, Doctor Nicole Hansbro, Doctor Kelly Asquith
Scheme Equipment Grant
Role Investigator
Funding Start 2009
Funding Finish 2009
GNo G0189851
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

20084 grants / $564,200

Innate immune factors regulate steroid-resistant airways hyperreactivity and asthma$503,250

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Doctor Ming Yang
Scheme Project Grant
Role Lead
Funding Start 2008
Funding Finish 2010
GNo G0187617
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

Individually ventilated cages (IVC) and associated ventilator, holding boxes and water bottles$35,000

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Professor Phil Hansbro, Professor Joerg Mattes, Doctor Simon Phipps, Doctor Ming Yang, Doctor Nicole Hansbro, Doctor Kelly Asquith
Scheme Equipment Grant
Role Investigator
Funding Start 2008
Funding Finish 2008
GNo G0188541
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

MicroRNA and antagomirs in the regulation and suppression of interferon (IFN)-g and lipopolysaccharide (LPS) induced steroid-resistant airways hyperreactivity$24,250

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Ming Yang, Laureate Professor Paul Foster
Scheme Project Grant
Role Lead
Funding Start 2008
Funding Finish 2008
GNo G0188474
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

The Thoracic Society of Australia and New Zealand Annual Scientific Meeting, Melbourne Australia, 30/3/2008 - 2/4/2008$1,700

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Doctor Ming Yang
Scheme Travel Grant
Role Lead
Funding Start 2008
Funding Finish 2008
GNo G0188618
Type Of Funding Internal
Category INTE
UON Y

20061 grants / $1,500

15th World Congress of pharmacology july 2-7, 2006$1,500

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Doctor Ming Yang
Scheme Travel Grant
Role Lead
Funding Start 2006
Funding Finish 2006
GNo G0186492
Type Of Funding Internal
Category INTE
UON Y

20053 grants / $2,228,601

Drug targets from new animal models$2,030,948

Funding body: CRC for Asthma

Funding body CRC for Asthma
Project Team Laureate Professor Paul Foster, Professor Phil Hansbro, Professor Joerg Mattes, Doctor Ming Yang, Dr Simon Phipps
Scheme Research Grant
Role Investigator
Funding Start 2005
Funding Finish 2011
GNo G0185860
Type Of Funding CRC - Cooperative Research Centre
Category 4CRC
UON Y

Understanding the role of IL-13 in the pathogenesis of asthma$168,173

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Doctor Ming Yang
Scheme Postdoctoral Research Fellowship
Role Lead
Funding Start 2005
Funding Finish 2007
GNo G0184063
Type Of Funding Internal
Category INTE
UON Y

Investigating the role of IL-13 induced arginas I activity in the development of allergic lung disease$29,480

Funding body: Ramaciotti Foundations

Funding body Ramaciotti Foundations
Project Team Doctor Ming Yang
Scheme Major Equipment Award
Role Lead
Funding Start 2005
Funding Finish 2005
GNo G0185636
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y
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Research Supervision

Number of supervisions

Completed4
Current1

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2017 PhD Innate Type 2 Responses and Viral-Induced Asthma Exacerbation 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
2021 PhD Understanding the Pathogenesis of Steroid-resistant Exacerbation of Allergic Airways Disease PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle Principal Supervisor
2017 PhD Modeling of Respiratory Syncytial Virus-induced Exacerbation of Allergic Airways Disease PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle Principal Supervisor
2017 PhD Understanding the Mechanisms of Bacterial-Induced Exacerbation of Allergic Airways Disease in a Mouse Model PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle Principal Supervisor
2014 PhD Respiratory Innate Immune Factors Regulate Steroid-resistant Airway Hyperreactivity and Asthma PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle Principal Supervisor
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Dr Ming Yang

Position

Senior Lecturer
School of Biomedical Sciences and Pharmacy
College of Health, Medicine and Wellbeing

Focus area

Immunology and Microbiology

Contact Details

Email ming.yang@newcastle.edu.au
Phone (02) 40420183

Office

Room Level 2, Immunology & Microbiology
Building HMRI Building
Location HMRI Building

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