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Dr Hock Tay

NHMRC Fellow

School of Biomedical Sciences and Pharmacy

Immunity and Respiratory Health

Dr Hock Tay’s research examines how and why airway infections can be so problematic for patients with chronic respiratory diseases.

Dr Hock Tay

“I was always interested in infection and immunity – in particular how infection moderates the immune system. It's interesting because sometimes when you have infection in patients with chronic lung disease, they have exacerbation of their condition."

“I’m focusing on how pathogens can manipulate the immune response to cause this exacerbation of disease.”

An emerging field of research

According to the central dogma of biology, in order for genes to work (and therefore for cells to be functional) the gene DNA has to be transcribed into RNA, which is translated into protein.

For a long time, it was thought that these proteins did all the important work within the cell. But throughout the past few decades, this central dogma has been turned upside-down.

Researchers have seen that RNA can have a functional role completely aside from their protein-coding function. There is also non-coding RNA that can function within the cell to alter cell activity.

A whole new area of research onto these ‘non-coding RNAs’ has blossomed. One particular type of non-coding RNA are known as microRNAs, of which there are thousands. Each microRNA has a different role – many of which are yet to be described. Importantly, one microRNA has the potential to modulate the level many coding-RNA and thus regulate the level of a range of proteins and integrated signalling networks.

“When I started looking at microRNAs around 10 years ago, their role in complex biological processes was just emerging – some non-coding was even thought to be ‘junk’. It’s only recently with new technologies that allow us to identify all the different microRNAs, that we can see how they are dysregulated in lots of diseases, as well as used in infection.”

“What's so interesting about them is that they can regulate multiple pathways. So that could be really important in disease pathogenesis.”

Hock first heard about these somewhat strange molecules during one of Laureate Professor Paul Foster’s lectures during his Biomedical Science degree at UON.

“Nothing much was known about them, so I was really curious!”

Hock approached Paul about working in his lab throughout his Summer Scholarship, and was excited to get started in the field of RNA and immunology.

“I’d actually applied to work with Paul on microRNAs for my undergraduate research project – but he had already taken on his students for the year so I had to go to a different lab."

“That was a great experience, but I knew that immunology was what I really wanted to work on.”

Regulating the immune cell response

During infection, the early immune response clears the pathogens, while adaptive immune response is called upon if the infection persists or reoccurs.

Throughout his PhD, Hock was focussing on the early responses to infection, as these drive inflammations that cause exacerbation of lung disease.

“The focus was on how these immune cells come in during the early stage, and how that changes the molecular miRNA signatures inside the cells.”

Hock focussed on a few select microRNAs and their role in the immune response, including miRNA-328.

“We found that is acts like a brake for the immune cells. Before infection, miRNA-328 stops the immune cells from becoming active so they’re not just going around destroying everything. Then during an infection, the levels of miRNA-328 drop, and we see upregulation of the immune response. The drop in miRNA-328 enhances the uptake of bacteria into the immune cell to be destroyed.”

New horizons

In 2016, Hock commenced his prestigious NHMRC Early Career fellowship, which he was awarded to continue his study into the role of non-coding RNAs in respiratory disease.

“I wasn't expecting it. It was a relief really - I can now plan for longer term projects instead of smaller projects which only run for one or two years.”

Throughout his fellowship, Hock will be moving on to study an entirely new group of non-coding RNA: long-non-coding RNAs.

“Where microRNAs are about 23 nucleotides (genetic units) long, long-non-coding RNAs are longer than 200. The mechanisms are completely different and they are actually even harder to study. But a lot of the skills I developed throughout my PhD will still be very useful. I’m really using my PhD as a building block for this project.”

With this fellowship, the University granted Hock two PhD scholarships, and he is taking on his own students for the very first time.

“Everyone tells me having students is going to be challenging but I'm excited about it. I'm excited about the opportunity of teaching someone and at the same time I’m pretty sure I can learn from them too.”

Immunity and Respiratory Health

Dr Hock Tay’s research examines how and why airway infections can be so problematic for patients with chronic respiratory diseases.

Read more

Career Summary

Biography

Dr Hock Tay obtained his PhD in Immunology & Microbiology in 2014. In 2015, he received NHMRC Peter Doherty Early Career Fellowship to undertake his post-doctoral research training in Hunter Medical Research Institute at The University of Newcastle, Australia under supervision of Laureate Professor Paul Foster. His researches focus on translational studies using murine model and clinical samples to study the role of the innate immune response and non-coding RNA in regulation of inflammatory responses in lung diseases. Dr Hock Tay has expertise and knowledge in the field of infectious and chronic inflammatory diseases of the lung, immunology, cytokine biology and non-coding RNA. He has 8 years experience in experimental work such as cell culture (primary cells and cell lines), isolation of primary cells, techniques with murine models of respiratory diseases including pharmacological and physiological studies. He has extensive experience in molecular techniques, RNA isolation and protein quantification. He has also established techniques to identify mRNA that are targets for miRNAs in macrophages, by using a biotin-streptavidin pull down approach, followed by RNAseq and bioinformatics techniques.


Qualifications

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

Keywords

  • Asthma
  • Immunology
  • Infectious diseases
  • Cytokines
  • Non-coding RNAs

Languages

  • English (Fluent)
  • Mandarin (Fluent)
  • Malay (Fluent)
  • Cantonese (Fluent)

Fields of Research

Code Description Percentage
110203 Respiratory Diseases 50
110704 Cellular Immunology 50

Professional Experience

UON Appointment

Title Organisation / Department
NHMRC Fellow 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 (19 outputs)

Year Citation Altmetrics Link
2018 Mateer SW, Mathe A, Bruce J, Liu G, Maltby S, Fricker M, et al., 'IL-6 Drives Neutrophil-Mediated Pulmonary Inflammation Associated with Bacteremia in Murine Models of Colitis.', Am J Pathol, 188 1625-1639 (2018)
DOI 10.1016/j.ajpath.2018.03.016
Co-authors Steven Maltby, Michael Fricker, Jay Horvat, Marjorie Walker, Gang Liu, Andrea Mathe, Simon Keely, Philip Hansbro, Paul Foster
2018 Maltby S, Lochrin AJ, Bartlett B, Tay HL, Weaver J, Poulton IJ, et al., 'Osteoblasts Are Rapidly Ablated by Virus-Induced Systemic Inflammation following Lymphocytic Choriomeningitis Virus or Pneumonia Virus of Mice Infection in Mice', Journal of Immunology, 200 632-642 (2018) [C1]

Copyright © 2018 by The American Association of Immunologists, Inc. A link between inflammatory disease and bone loss is now recognized. However, limited data exist on the impact ... [more]

Copyright © 2018 by The American Association of Immunologists, Inc. A link between inflammatory disease and bone loss is now recognized. However, limited data exist on the impact of virus infection on bone loss and regeneration. Bone loss results from an imbalance in remodeling, the physiological process whereby the skeleton undergoes continual cycles of formation and resorption. The specific molecular and cellular mechanisms linking virus-induced inflammation to bone loss remain unclear. In the current study, we provide evidence that infection of mice with either lymphocytic choriomeningitis virus (LCMV) or pneumonia virus of mice (PVM) resulted in rapid and substantial loss of osteoblasts from the bone surface. Osteoblast ablation was associated with elevated levels of circulating inflammatory cytokines, including TNF-a, IFN-g, IL-6, and CCL2. Both LCMV and PVM infections resulted in reduced osteoblast-specific gene expression in bone, loss of osteoblasts, and reduced serum markers of bone formation, including osteocalcin and procollagen type 1 N propeptide. Infection of Rag-1-deficient mice (which lack adaptive immune cells) or specific depletion of CD8+T lymphocytes limited osteoblast loss associated with LCMV infection. By contrast, CD8+T cell depletion had no apparent impact on osteoblast ablation in association with PVM infection. In summary, our data demonstrate dramatic loss of osteoblasts in response to virus infection and associated systemic inflammation. Further, the inflammatory mechanisms mediating viral infection-induced bone loss depend on the specific inflammatory condition.

DOI 10.4049/jimmunol.1700927
Citations Scopus - 1Web of Science - 1
Co-authors Steven Maltby, 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]

Copyright © 2017 by The American Association of Immunologists, Inc. Respiratory syncytial virus (RSV) infection induces asthma exacerbations, which leads to worsening of clinical ... [more]

Copyright © 2017 by The American Association of Immunologists, Inc. 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 - 1Web of Science - 1
Co-authors Steven Maltby, Paul Foster, Ming Yang
2017 Foster PS, Maltby S, Rosenberg HF, Tay HL, Hogan SP, Collison AM, et al., 'Modeling T

© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd In this review, we highlight experiments conducted in our laboratories that have elucidated functional... [more]

© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd 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 - 5Web of Science - 6
Co-authors Nicole Hansbro, Gerard Kaiko, Adam Collison, Ming Yang, Paul Foster, Steven Maltby, Joerg Mattes, Philip Hansbro
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, 22 874-885 (2017) [C1]

© 2017 Asian Pacific Society of Respirology Severe asthma has significant disease burden and results in high healthcare costs. While existing therapies are effective for the major... [more]

© 2017 Asian Pacific Society of Respirology 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 - 6Web of Science - 6
Co-authors Paul Foster, Steven Maltby, Ming Yang
2017 Liu G, Cooley MA, Nair PM, Donovan C, Hsu AC, Jarnicki AG, et al., 'Airway remodelling and inflammation in asthma are dependent on the extracellular matrix protein fibulin-1c', JOURNAL OF PATHOLOGY, 243 510-523 (2017) [C1]
DOI 10.1002/path.4979
Citations Scopus - 2Web of Science - 3
Co-authors Nicole Hansbro, Jay Horvat, Philip Hansbro, Christopher Grainge, Darryl Knight, Chantal Donovan, Paul Foster, Peter Wark, Gang Liu, Alan Hsu
2017 Tay HL, 'Th22 Cells Form a Distinct Th Lineage from Th17 Cells In Vitro with Unique Transcriptional Properties and Tbet-Dependent Th1 Plasticity.', JOURNAL OF IMMUNOLOGY, 198 2182-2190 (2017) [C1]
DOI 10.4049/jimmunol.1601480
Citations Scopus - 8Web of Science - 8
Co-authors Paul Foster, Steven Maltby, Gerard Kaiko
2016 Tay H, Wark PAB, Bartlett NW, 'Advances in the treatment of virus-induced asthma', Expert Review of Respiratory Medicine, 10 629-641 (2016) [C1]

© 2016 Informa UK Limited, trading as Taylor & Francis Group. ABSTRACT: Viral exacerbations continue to represent the major burden in terms of morbidity, mortality and healt... [more]

© 2016 Informa UK Limited, trading as Taylor & Francis Group. ABSTRACT: Viral exacerbations continue to represent the major burden in terms of morbidity, mortality and health care costs associated with asthma. Those at greatest risk for acute asthma are those with more severe airways disease and poor asthma control. It is this group with established asthma in whom acute exacerbations triggered by virus infections remain a serious cause of increased morbidity. A range of novel therapies are emerging to treat asthma and in particular target this group with poor disease control, and in most cases their efficacy is now being judged by their ability to reduce the frequency of acute exacerbations. Critical for the development of new treatment approaches is an improved understanding of virus-host interaction in the context of the asthmatic airway. This requires research into the virology of the disease in physiological models in conjunction with detailed phenotypic characterisation of asthma patients to identify targets amenable to therapeutic intervention.

DOI 10.1080/17476348.2016.1180249
Citations Scopus - 2Web of Science - 1
Co-authors Peter Wark, Nathan Bartlett
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]

Copyright © 2016 by The American Association of Immunologists, Inc. MicroRNAs (miRNAs) are short noncoding RNAs that regulate a broad spectrum of biological processes, including i... [more]

Copyright © 2016 by The American Association of Immunologists, Inc. 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 - 14Web of Science - 16
Co-authors Paul Foster, Ming Yang
2016 Maltby S, Plank M, Tay HL, Collison A, Foster PS, 'Targeting MicroRNA function in respiratory diseases: Mini-review', Frontiers in Physiology, 7 (2016) [C1]
DOI 10.3389/fphys.2016.00021
Citations Scopus - 25Web of Science - 20
Co-authors Steven Maltby, Paul Foster, Adam Collison
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 - 1Web of Science - 2
Co-authors Paul Foster, Ming Yang
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 - 1
Co-authors Joerg Mattes, Gerard Kaiko, Philip Hansbro, Ming Yang, Steven Maltby, Paul Foster
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]

© 2015 American Academy of Allergy, Asthma & Immunology. Background Steroid-resistant asthma is a major clinical problem that is linked to activation of innate immune cells.... [more]

© 2015 American Academy of Allergy, Asthma & Immunology. 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 - 30Web of Science - 29
Co-authors Steven Maltby, Paul Foster, Joerg Mattes, Ming Yang
2015 Plank MW, Maltby S, Tay HL, Stewart J, Eyers F, Hansbro PM, Foster PS, 'MicroRNA Expression Is Altered in an Ovalbumin-Induced Asthma Model and Targeting miR-155 with Antagomirs Reveals Cellular Specificity.', PloS one, 10 1-25 (2015) [C1]
DOI 10.1371/journal.pone.0144810
Citations Scopus - 17Web of Science - 19
Co-authors Philip Hansbro, Steven Maltby, Paul Foster
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]

© 2015 Tay et al. Pathogenic bacterial infections of the lung are life threatening and underpin chronic lung diseases. Current treatments are often ineffective potentially due to ... [more]

© 2015 Tay et al. 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 - 25Web of Science - 29
Co-authors Philip Hansbro, Steven Maltby, Paul Foster, Gerard Kaiko, Joerg Mattes, Ming Yang
2014 Maltby S, Hansbro NG, Tay HL, Stewart J, Plank M, Donges B, et al., 'Production and differentiation of myeloid cells driven by proinflammatory cytokines in response to acute pneumovirus infection in mice.', J Immunol, 193 4072-4082 (2014) [C1]
DOI 10.4049/jimmunol.1400669
Citations Scopus - 11Web of Science - 10
Co-authors Steven Maltby, Nicole Hansbro, Paul Foster
2014 Tay HL, Plank M, Collison A, Mattes J, Kumar RK, Foster PS, 'MicroRNA: Potential biomarkers and therapeutic targets for allergic asthma?', Annals of Medicine, 46 633-639 (2014) [C1]

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

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

DOI 10.3109/07853890.2014.958196
Citations Scopus - 15Web of Science - 12
Co-authors Adam Collison, Paul Foster, Joerg Mattes
2013 Foster PS, Plank MW, Collison AM, Tay HL, Kaiko GE, Li J, et al., 'The emerging role of microRNAs in regulating immune and inflammatory responses in the lung', Immunological Reviews, 253 198-215 (2013) [C1]
Citations Scopus - 54Web of Science - 57
Co-authors Gerard Kaiko, Philip Hansbro, Paul Foster, Ming Yang, Adam Collison, Joerg Mattes
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 - 12Web of Science - 5
Co-authors Ming Yang, Philip Hansbro, Paul Foster
Show 16 more journal articles

Conference (5 outputs)

Year Citation Altmetrics Link
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 Alan Hsu, Adam Collison, Gerard Kaiko, Ming Yang, Philip Hansbro, Joerg Mattes, Paul Foster, Chantal Donovan
2013 Tay H, Kaiko G, Hansbro P, Foster P, 'The role of miRNA in regulating bacterial clearance', JOURNAL OF IMMUNOLOGY, Honolulu, HI (2013) [E3]
Citations Web of Science - 1
Co-authors Philip Hansbro, Paul Foster, Gerard Kaiko
2012 Kaiko GE, Phipps S, Plank MW, Tay HL, Lam CE, Foster PS, 'Inhibition of microRNA reverses CD8 T cell exhaustion and improves immunity against respiratory virus infection', Respirology, Canberra, ACT (2012) [E3]
Co-authors Gerard Kaiko, Paul Foster
2012 Tay HL, Kaiko GE, Plank MW, Mattes J, Hansbro PM, Foster PS, 'MiRNAs regulate bacterial infection in lungs', Respirology, Canberra, ACT (2012) [E3]
Co-authors Gerard Kaiko, Philip Hansbro, Paul Foster, Joerg Mattes
2011 Foster PS, Tay HL, Kaiko GE, Plank MW, Mattes J, Hansbro PM, 'MiRNA and its roles in regulating bacterial infection in lungs', American Journal of Respiratory and Critical Care Medicine, Denver, CO (2011) [E3]
Co-authors Joerg Mattes, Paul Foster, Gerard Kaiko, Philip Hansbro
Show 2 more conferences
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Grants and Funding

Summary

Number of grants 6
Total funding $1,139,391

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


20172 grants / $756,986

Characterising the pro-inflammatory role of IL-36¿/IL-36R in pathogen-induced exacerbations of asthma and COPD$746,986

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
Scheme Project Grant
Role Investigator
Funding Start 2017
Funding Finish 2020
GNo G1600081
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

Countess II FL$10,000

Funding body: NSW Ministry of Health

Funding body NSW Ministry of Health
Project Team Doctor Malcolm Starkey, Doctor Adam Collison, Doctor Hock Tay, Doctor Aniruddh Deshpande, Doctor Gang Liu, Doctor Jemma Mayall
Scheme Medical Research Support Program (MRSP)
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1701221
Type Of Funding C2220 - Aust StateTerritoryLocal - Other
Category 2220
UON Y

20163 grants / $362,405

The role of long non-coding RNA in regulating lung immunity and inflammation$321,920

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Doctor Hock Tay
Scheme Early Career Fellowships
Role Lead
Funding Start 2016
Funding Finish 2020
GNo G1500549
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

Exploring Novel Therapies for Cystic Fibrosis$22,500

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Hock Tay, Laureate Professor Paul Foster, Mr Max Plank, Doctor Steven Maltby
Scheme Project Grant
Role Lead
Funding Start 2016
Funding Finish 2016
GNo G1600577
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Research Advantage Early Career Researcher Equipment Grant $17,985

Funding body: The University of Newcastle - Research and Innovation Division

Funding body The University of Newcastle - Research and Innovation Division
Project Team

Malcolm Starkey, Chantal Donovan, Richard Kim, Andrew Reid, Hock Tay

Scheme Research Advantage Funding
Role Investigator
Funding Start 2016
Funding Finish 2016
GNo
Type Of Funding Not Known
Category UNKN
UON N

20141 grants / $20,000

Virus Infections Change the Bone Marrow: Effects on Immunity, Bone Development and Inflammatory Disease$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Steven Maltby, Mr Max Plank, Doctor Hock Tay, Laureate Professor Paul Foster
Scheme Project Grant
Role Investigator
Funding Start 2014
Funding Finish 2014
GNo G1401394
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y
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Research Supervision

Number of supervisions

Completed0
Current3

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2017 PhD Understanding the Link Between Fungal Exposure and Severe Asthma PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2017 PhD Characterising Proinflammatory Role of IL-36y/IL-36R in Pathogen-induced Exacerbations of Asthma PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2017 PhD Role of Non-coding RNAs (ncRNAs) in Cystic Fibrosis Background PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
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News

NHMRC Early Career Fellowship 2016

November 13, 2015

Dr Hock Tay has been awarded more than $314,000 in NHMRC Early Career Fellowships funding commencing in 2016 for his research in The role of long non-coding

Dr Hock Tay

Position

NHMRC Fellow
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Contact Details

Email hock.tay@newcastle.edu.au
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