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Dr Steven Maltby

Research Academic

School of Nursing and Midwifery

Career Summary

Biography

I currently work 3 days/week with the Centre for Advanced Training Systems, developing innovative platforms to use virtual and augmented reality in teaching and training.

I remain the Executive Officer with the Excellence in Severe Asthma (www.severeasthma.org.au). In this role, I am actively involved in science communications and logistics and administration of the research network.

Past Experience:

I initially came to Australia and the University of Newcastle on a Post-doctoral Research Fellowship, with Laureate Professor Paul Foster . My  research focused on characterizing changes in the bone marrow during disease and infection. During a virus infection, an immune response is rapidly induced. This immune response is required to kill the virus and infected cells.  However, the immune response often also causes a lot of the damage and pathology that is observed. The aim of my studies was characterise what happens when a virus is first detected by the immune system, including systemic changes in the bone marrow. The bone marrow houses immune cell progentors that give rise to mature immune cells, as well as structural cells that are important for maintaining mineral bone.

I completed PhD studies with Dr Kelly McNagny at The Biomedical Research Centre, University of British Columbia in Vancouver, BC, Canada. My research focused on the role of CD34 (and the related molecule podocalyxin) in immune responses, using mouse models of disease. Those studies identified the importance of CD34 for efficient eosinophil and mast cell migration to sites of inflammation during disease. Further, I demonstrated that loss of CD34 expression (using transgenic Cd34-/- animals) resulted in reduced disease severity in mouse models of asthma and ulcerative colitis.

Research Expertise
Main Research Focus Areas: Bone Marrow Responses, Immune Cell Activation and Migration, Virus Infections, Asthma & Respiratory Disease, Teaching Platforms and Technologies

Teaching Expertise
Immunology


Qualifications

  • PhD, University of British Columbia - Canada
  • Bachelor of Science, University of British Columbia - Canada

Keywords

  • Asthma
  • Augmented Reality
  • Bone Biology
  • Bone Marrow
  • Disease Models
  • Hematopoiesis
  • Immunology
  • Infection
  • Teaching
  • Training
  • Virtual Reality
  • Virus

Languages

  • English (Fluent)

Fields of Research

Code Description Percentage
130101 Continuing and Community Education 60
110309 Infectious Diseases 20
110799 Immunology not elsewhere classified 20

Professional Experience

UON Appointment

Title Organisation / Department
Research Academic

Science Communications & Research Academic (www.severeasthma.org.au)

University of Newcastle
School of Nursing and Midwifery
Australia
Casual Academic University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia

Academic appointment

Dates Title Organisation / Department
1/01/2012 - 5/05/2016 University of Newcastle Research Fellow

University of Newcastle Research Fellowship

University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia
1/07/2010 - 1/09/2011 Post-doctoral fellow University of British Columbia
The Biomedical Research Centre
Canada

Awards

Research Award

Year Award
2012 Postdoctoral Research Fellowship
Canadian Institutes of Health Research
2012 Postdoctoral Research Fellowship
University of Newcastle
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Publications

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


Chapter (3 outputs)

Year Citation Altmetrics Link
2019 Girkin J, Maltby S, Singanayagam A, Bartlett N, Malia P, 'In vivo experimental models of infection and disease', Rhinovirus infections. Rethinking impact on human health and disease, Elsevier, London 195-238 (2019)
Co-authors Nathan Bartlett
2015 Maltby S, Plank M, Ptaschinski C, Mattes J, Foster PS, 'MicroRNA function in mast cell biology: Protocols to characterize and modulate MicroRNA expression', Mast Cells: Methods and Protocols, Springer, New York 287-304 (2015) [B1]
DOI 10.1007/978-1-4939-1568-2_18
Citations Scopus - 6
Co-authors Joerg Mattes, Paul Foster
2013 Maltby S, McNagny KM, Ackerman SJ, Du J, Mori Y, Iwasaki H, et al., 'Eosinophilopoiesis', Eosinophils in Health and Disease 73-119 (2013) [B2]
DOI 10.1016/B978-0-12-394385-9.00005-5
Citations Scopus - 1

Journal article (32 outputs)

Year Citation Altmetrics Link
2019 Liu G, Mateer SW, Hsu A, Goggins BJ, Tay H, Mathe A, et al., 'Platelet activating factor receptor regulates colitis-induced pulmonary inflammation through the NLRP3 inflammasome', Mucosal Immunology, 12 862-873 (2019)

© 2019, Society for Mucosal Immunology. Extra-intestinal manifestations (EIM) are common in inflammatory bowel disease (IBD). One such EIM is sub-clinical pulmonary inflammation, ... [more]

© 2019, Society for Mucosal Immunology. Extra-intestinal manifestations (EIM) are common in inflammatory bowel disease (IBD). One such EIM is sub-clinical pulmonary inflammation, which occurs in up to 50% of IBD patients. In animal models of colitis, pulmonary inflammation is driven by neutrophilic infiltrations, primarily in response to the systemic bacteraemia and increased bacterial load in the lungs. Platelet activating factor receptor (PAFR) plays a critical role in regulating pulmonary responses to infection in conditions, such as chronic obstructive pulmonary disease and asthma. We investigated the role of PAFR in pulmonary EIMs of IBD, using dextran sulfate sodium (DSS) and anti-CD40 murine models of colitis. Both models induced neutrophilic inflammation, with increased TNF and IL-1ß levels, bacterial load and PAFR protein expression in mouse lungs. Antagonism of PAFR decreased lung neutrophilia, TNF, and IL-1ß in an NLRP3 inflammasome-dependent manner. Lipopolysaccharide from phosphorylcholine (ChoP)-positive bacteria induced NLRP3 and caspase-1 proteins in human alveolar epithelial cells, however antagonism of PAFR prevented NLRP3 activation by ChoP. Amoxicillin reduced bacterial populations in the lungs and reduced NLRP3 inflammasome protein levels, but did not reduce PAFR. These data suggest a role for PAFR in microbial pattern recognition and NLRP3 inflammasome signaling in the lung.

DOI 10.1038/s41385-019-0163-3
Citations Scopus - 1
Co-authors Philip Hansbro, Bridie Goggins, Peter Wark, Andrea Mathe, Alan Hsu, Simon Keely, Paul Foster, Hock Tay, Michael Fricker
2018 Mateer SW, Mathe A, Bruce J, Liu G, Maltby S, Fricker M, et al., 'IL-6 Drives Neutrophil-Mediated Pulmonary Inflammation Associated with Bacteremia in Murine Models of Colitis', American Journal of Pathology, 188 1625-1639 (2018) [C1]

© 2018 American Society for Investigative Pathology Inflammatory bowel disease (IBD) is associated with several immune-mediated extraintestinal manifestations. More than half of a... [more]

© 2018 American Society for Investigative Pathology Inflammatory bowel disease (IBD) is associated with several immune-mediated extraintestinal manifestations. More than half of all IBD patients have some form of respiratory pathology, most commonly neutrophil-mediated diseases, such as bronchiectasis and chronic bronchitis. Using murine models of colitis, we aimed to identify the immune mechanisms driving pulmonary manifestations of IBD. We found increased neutrophil numbers in lung tissue associated with the pulmonary vasculature in both trinitrobenzenesulfonic acid¿ and dextran sulfate sodium¿induced models of colitis. Analysis of systemic inflammation identified that neutrophilia was associated with bacteremia and pyrexia in animal models of colitis. We further identified IL-6 as a systemic mediator of neutrophil recruitment from the bone marrow of dextran sulfate sodium animals. Functional inhibition of IL-6 led to reduced systemic and pulmonary neutrophilia, but it did not attenuate established colitis pathology. These data suggest that systemic bacteremia and pyrexia drive IL-6 secretion, which is a critical driver for pulmonary manifestation of IBD. Targeting IL-6 may reduce neutrophil-associated extraintestinal manifestations in IBD patients.

DOI 10.1016/j.ajpath.2018.03.016
Citations Scopus - 3Web of Science - 2
Co-authors Marjorie Walker, Jay Horvat, Robert Callister, Philip Hansbro, Simon Keely, Andrea Mathe, Michael Fricker, Hock Tay, Bridie Goggins, 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 - 5Web of Science - 4
Co-authors Hock Tay, Paul Foster
2018 Jones KA, Maltby S, Plank MW, Kluge M, Nilsson M, Foster PS, Walker FR, 'Peripheral immune cells infiltrate into sites of secondary neurodegeneration after ischemic stroke', Brain, Behavior, and Immunity, 67 299-307 (2018) [C1]

© 2017 Elsevier Inc. Experimental stroke leads to microglia activation and progressive neuronal loss at sites of secondary neurodegeneration (SND). These lesions are remote from, ... [more]

© 2017 Elsevier Inc. Experimental stroke leads to microglia activation and progressive neuronal loss at sites of secondary neurodegeneration (SND). These lesions are remote from, but synaptically connected to, primary infarction sites. Previous studies have demonstrated that immune cells are present in sites of infarction in the first hours and days after stroke, and are associated with increased neurodegeneration in peri-infarct regions. However, it is not known whether immune cells are also present in more distal sites where SND occurs. Our study aimed to investigate whether immune cells are present in sites of SND and, if so, how these cell populations compare to those in the peri-infarct zone. Cells were isolated from the thalamus, the main site of SND, and remaining brain tissue 14 days post-stroke. Analysis was performed using flow cytometry to quantify microglia, myeloid cell and lymphocyte numbers. We identified a substantial infiltration of immune cells in the ipsilateral (stroked) compared to the contralateral (control) thalamus, with a significant increase in the percentage of CD4+ and CD8+ T cells. This result was further quantified using immunofluorescent labelling of fixed tissue. In the remaining ipsilateral hemisphere tissue, there were significant increases in the frequency of CD4+ and CD8+ T lymphocytes, B lymphocytes, Ly6G+ neutrophils and both Ly6G-Ly6CLO and Ly6G-Ly6CHI monocytes. Our results indicate that infiltrating immune cells persist in ischemic tissue after the acute ischemic phase, and are increased in sites of SND. Importantly, immune cells have been shown to play pivotal roles in both damage and repair processes after stroke. Our findings indicate that immune cells may also be involved in the pathogenesis of SND and further clinical studies are warranted to characterise the nature of inflammatory cell infiltrates in human disease.

DOI 10.1016/j.bbi.2017.09.006
Citations Scopus - 18Web of Science - 17
Co-authors Paul Foster, Rohan Walker, Michael Nilsson
2018 Porsbjerg C, Sverrild A, Baines KJ, Searles A, Maltby S, Foster PS, et al., 'Advancing the management of obstructive airways diseases through translational research.', Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 48 493-501 (2018) [C1]
DOI 10.1111/cea.13112
Co-authors Andrew Searles, Peter Gibson, Katherine Baines, Paul Foster
2018 McDonald VM, Maltby S, Gibson PG, 'Severe asthma: We can fix it? We can try!', RESPIROLOGY, 23 260-261 (2018)
DOI 10.1111/resp.13249
Citations Scopus - 1Web of Science - 1
Co-authors Vanessa Mcdonald, Peter Gibson
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 - 5Web of Science - 4
Co-authors Paul Foster, Hock Tay, 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 - 17Web of Science - 15
Co-authors Gerard Kaiko, Adam Collison, Ming Yang, Paul Foster, Hock Tay, Joerg Mattes, Nicole Hansbro, 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 - 9Web of Science - 7
Co-authors Paul Foster, Ming Yang, Hock Tay
2017 McDonald VM, Maltby S, Reddel HK, King GG, Wark PAB, Smith L, et al., 'Severe asthma: Current management, targeted therapies and future directions A roundtable report', Respirology, 22 53-60 (2017) [C1]

© 2016 Asian Pacific Society of Respirology Asthma is a chronic respiratory disease characterized by respiratory symptoms, airway inflammation, airway obstruction and airway hyper... [more]

© 2016 Asian Pacific Society of Respirology Asthma is a chronic respiratory disease characterized by respiratory symptoms, airway inflammation, airway obstruction and airway hyper-responsiveness. Asthma is common and directly affects 10% of Australians, 1¿5% of adults in Asia and 300 million people worldwide. It is a heterogeneous disorder with many clinical, molecular, biological and pathophysiological phenotypes. Current management strategies successfully treat the majority of patients with asthma who have access to them. However, there is a subset of an estimated 5¿10% of patients with asthma who have severe disease and are disproportionately impacted by symptoms, exacerbations and overall illness burden. The care required for this relatively small proportion of patients is also significant and has a major impact on the healthcare system. A number of new therapies that hold promise for severe asthma are currently in clinical trials or are entering the Australian and international market. However, recognition of severe asthma in clinical practice is variable, and there is little consensus on the best models of care or how to integrate emerging and often costly therapies into current practice. In this article, we report on roundtable discussions held with severe asthma experts from around Australia, and make recommendations about approaches for better patient diagnosis and assessment. We assess current models of care for patient management and discuss how approaches may be optimized to improve patient outcomes. Finally, we propose mechanisms to assess new therapies and how to best integrate these approaches into future treatment.

DOI 10.1111/resp.12957
Citations Scopus - 20Web of Science - 23
Co-authors Peter Gibson, Peter Wark, Vanessa Mcdonald
2017 Maltby S, Gibson PG, Powell H, McDonald VM, 'Omalizumab Treatment Response in a Population With Severe Allergic Asthma and Overlapping COPD', Chest, 151 78-89 (2017) [C1]

© 2016 American College of Chest Physicians Background Asthma and COPD are common airway diseases. Individuals with overlapping asthma and COPD experience increased health impairm... [more]

© 2016 American College of Chest Physicians Background Asthma and COPD are common airway diseases. Individuals with overlapping asthma and COPD experience increased health impairment and severe disease exacerbations. Efficacious treatment options are required for this population. Omalizumab (anti-IgE) therapy is effective in patients with severe persistent asthma, but limited data are available on efficacy in populations with overlapping asthma and COPD. Methods Data from the Australian Xolair Registry were used to compare treatment responses in individuals with asthma-COPD overlap with responses in patients with severe asthma alone. Participants were assessed at baseline and after 6¿months of omalizumab treatment. We used several different definitions of asthma-COPD overlap. First, we compared participants with a previous physician diagnosis of COPD to participants with no COPD diagnosis. We then made¿comparisons based on baseline lung function, comparing participants with an FEV1 <¿80%¿predicted to those with an FEV1 > 80%¿predicted after bronchodilator use. In the population with an FEV1< 80%, analysis was further stratified based on smoking history. Results Omalizumab treatment markedly improved asthma control and health-related quality of life in all populations assessed based on the Asthma Control Questionnaire and Asthma Quality of Life Questionnaire scores. Omalizumab treatment did not improve lung function (FEV1, FVC, or FEV1/FVC ratio) in populations that were enriched for asthma-COPD overlap (diagnosis of COPD or FEV1¿< 80%/ever smokers). Conclusions Our study suggests that omalizumab improves asthma control and health-related quality of life in individuals with severe allergic asthma and overlapping COPD. These findings provide real-world efficacy data for this patient population and suggest that omalizumab is useful in the management of severe asthma with COPD overlap.

DOI 10.1016/j.chest.2016.09.035
Citations Scopus - 24Web of Science - 28
Co-authors Vanessa Mcdonald, Peter Gibson
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 - 18Web of Science - 16
Co-authors Paul Foster, Hock Tay, Gerard Kaiko
2016 Maltby S, Gibson P, Mattes J, McDonald VM, 'How to treat Severe Asthma Part 2 Management.', Australian Doctor, (2016)
Co-authors Peter Gibson, Vanessa Mcdonald, Joerg Mattes
2016 Maltby S, Gibson P, Mattes J, McDonald VM, 'How to treat Severe Asthma Part 1 Diagnosis', Australian Doctor, (2016)
Co-authors Vanessa Mcdonald, Peter Gibson, Joerg Mattes
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 - 17Web of Science - 17
Co-authors Katherine Baines, Ming Yang, Paul Foster, Jodie Simpson, Peter Gibson
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 - 31Web of Science - 29
Co-authors Paul Foster, Adam Collison, Hock Tay
2016 Wark PAB, Hew M, Maltby S, McDonald VM, Gibson PG, 'Diagnosis and investigation in the severe asthma clinic.', Expert Rev Respir Med, 10 491-503 (2016) [C1]
DOI 10.1586/17476348.2016.1165096
Citations Scopus - 10Web of Science - 11
Co-authors Peter Wark, Vanessa Mcdonald, Peter Gibson
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 - 6Web of Science - 6
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 Hock Tay, Philip Hansbro, Paul Foster, Joerg Mattes, Ming Yang, Gerard Kaiko
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 &amp; 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 - 39Web of Science - 38
Co-authors Ming Yang, Joerg Mattes, Hock Tay, Paul Foster
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 - 21Web of Science - 25
Co-authors Paul Foster, Philip Hansbro, 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]

© 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 - 30Web of Science - 34
Co-authors Ming Yang, Paul Foster, Gerard Kaiko, Joerg Mattes, Hock Tay, Philip Hansbro
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 - 13Web of Science - 13
Co-authors Hock Tay, Nicole Hansbro, Paul Foster
2013 Plank M, Maltby S, Mattes J, Foster PS, 'Targeting translational control as a novel way to treat inflammatory disease: The emerging role of MicroRNAs', Clinical and Experimental Allergy, 43 981-999 (2013) [C1]

Chronic inflammatory diseases (e.g. asthma and chronic obstructive pulmonary disease) are leading causes of morbidity and mortality world-wide and effective treatments are limited... [more]

Chronic inflammatory diseases (e.g. asthma and chronic obstructive pulmonary disease) are leading causes of morbidity and mortality world-wide and effective treatments are limited. These disorders can often be attributed to abnormal immune responses to environmental stimuli and infections. Mechanisms leading to inflammation are complex, resulting from interactions of structural cells and activation of both the adaptive and innate arms of the immune system. The activation of structural and immune cells involves both temporary and permanent changes in gene expression in these cells, which underpin chronic inflammation and tissue dysfunction. miRNAs are small non-coding RNAs increasingly being recognized to play important roles in the post-transcriptional regulation of gene expression in mammalian cells by regulating translation. Individual miRNAs can exert their effects by directly inhibiting the translation or stability of multiple mRNAs simultaneously. Thus, the expression or blockade of function of a single miRNA (miR) can result in pronounced alterations in protein expression within a given cell. Dysregulation of miRNA expression may subsequently alter cellular function, and in certain situations predispose to disease. Our current understanding of the role of miRNA in the regulation of inflammatory disease (e.g. allergic diseases) remains limited. In this review, we provide an overview of the current understanding of miRNA biogenesis and function, the roles miRNA play in the regulation of immune cell function and their potential contribution to inflammatory diseases. We also highlight strategies to alter miRNA function for experimental or therapeutic gain, and discuss the potential utility and limitations of targeting these molecules as anti-inflammatory strategies. © 2013 John Wiley & Sons Ltd.

DOI 10.1111/cea.12135
Citations Scopus - 36Web of Science - 40
Co-authors Paul Foster, Joerg Mattes
2013 Plank M, Maltby S, Mattes J, Foster PS, 'Targeting translational control as a novel way to treat inflammatory disease: the emerging role of microRNAs.', Clinical and Experimental Allergy, 43 981-999 (2013)
DOI 10.1111/cea.12170
Co-authors Joerg Mattes, Paul Foster
2012 Maltby SJ, Debruin EJ, Bennett J, Gold MJ, Tunis MC, Jian Z, et al., 'IL-7Ra and L-selectin, but not CD103 or CD34, are required for murine peanut-induced anaphylaxis', Allergy Asthma and Clinical Immunology, 8 15-25 (2012) [C1]
DOI 10.1186/1710-1492-8-15
Citations Scopus - 1Web of Science - 1
2011 Maltby SJ, Freeman S, Gold MJ, Baker JH, Minchinton AI, Gold MR, et al., 'Opposing Roles for CD34 in B16 Melanoma Tumor Growth Alter Early Stage Vasculature and Late Stage Immune Cell Infiltration', PLoS One, 6 e18160-e18160 (2011) [C1]
DOI 10.1371/journal.pone.0018160
Citations Scopus - 16Web of Science - 12
2010 Maltby SJ, Wohlfarth C, Gold M, Zbytnuik L, Hughes MR, McNagny KM, 'CD34 is required for infiltration of eosinophils into the colon and pathology associated with DSS-induced ulcerative colitis', American Journal of Pathology, 177 1244-1254 (2010) [C1]
DOI 10.2353/ajpath.2010.100191
Citations Scopus - 27Web of Science - 25
2010 Blanchet M-R, Gold M, Maltby SJ, Bennett J, Petri B, Kubes P, et al., 'Loss of CD34 leads to exacerbated autoimmune arthritis through increased vascular permeability', Journal of Immunology, 184 1292-1299 (2010) [C1]
DOI 10.4049/?jimmunol.0900808
Citations Scopus - 22Web of Science - 21
2010 Maltby SJ, Wong J, Berberovic Z, Birkenmeier CS, Haddon DJ, Garcha K, et al., 'A novel ENU-generated truncation mutation lacking the spectrin-binding and C-terminal regulatory domains of Ank1 models severe, hemolytic hereditary spherocytosis', Experimental Hematology, 39 601-610 (2010) [C1]
DOI 10.1016/j.exphem.2010.12.009
Citations Scopus - 21Web of Science - 18
2009 Maltby SJ, Hughes MR, Zbytnuik L, Paulson RF, McNagny KM, 'Podocalyxin selectively marks erythroid-committed progenitors during anemic stress but is dispensable for efficient recovery', Experimental Hematology, 37 10-18 (2009) [C1]
DOI 10.1016/j.exphem.2008.09.006
Citations Scopus - 6Web of Science - 6
2007 Blanchet M-R, Maltby SJ, Haddon DJ, Merkens H, Zbytnuik L, McNagny KM, 'CD34 facilitates the development of allergic asthma', Blood, 110 2005-2012 (2007) [C1]
Citations Scopus - 51Web of Science - 50
Show 29 more journal articles

Review (4 outputs)

Year Citation Altmetrics Link
2017 McDonald VM, Maltby S, Gibson PG, 'Severe asthma: Can we fix it? Prologue to seeking innovative solutions for severe asthma', RESPIROLOGY (2017)
DOI 10.1111/resp.12956
Citations Scopus - 1Web of Science - 3
Co-authors Vanessa Mcdonald, Peter Gibson
2016 Grainge CL, Maltby S, Gibson PG, Wark PAB, McDonald VM, 'Targeted therapeutics for severe refractory asthma: monoclonal antibodies', EXPERT REVIEW OF CLINICAL PHARMACOLOGY (2016)
DOI 10.1586/17512433.2016.1172208
Citations Scopus - 11Web of Science - 15
Co-authors Peter Gibson, Christopher Grainge, Vanessa Mcdonald, Peter Wark
2015 Mateer SW, Maltby S, Marks E, Foster PS, Horvat JC, Hansbro PM, Keely S, 'Potential mechanisms regulating pulmonary pathology in inflammatory bowel disease.', J Leukoc Biol (2015) [C1]
DOI 10.1189/jlb.3RU1114-563R
Citations Scopus - 8Web of Science - 7
Co-authors Jay Horvat, Philip Hansbro, Simon Keely, Paul Foster
2009 Maltby SJ, Khash K, McNagny KM, 'Mast cells in tumor growth: angiogenesis, tissue remodeling and immune-modulation', Biochimica et biophysica acta - Reviews on Cancer (2009) [D1]
Citations Scopus - 184Web of Science - 164
Show 1 more review

Conference (18 outputs)

Year Citation Altmetrics Link
2018 Mcdonald VM, Maltby S, Clark VL, Hew M, King GG, Oo S, et al., 'DEVELOPMENT OF THE SEVERE ASTHMA TOOLKIT: A CLINICAL WEBSITE RESOURCE FOR THE MANAGEMENT OF SEVERE TREATMENT-REFRACTORY ASTHMA', RESPIROLOGY (2018)
Citations Web of Science - 1
Co-authors Vanessa Clark, Peter Gibson, Vanessa Mcdonald
2017 Plank MW, Kaiko GE, Maltby S, Weaver J, Tay H, Shen W, et al., 'Th22 cells form a distinct th lineage from Th17 cells in vitro with unique transcriptional properties and Tbet-dependent Th1 plasticity', ALLERGY, Helsinki, FINLAND (2017)
Co-authors Gerard Kaiko, Paul Foster
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 Jodie Simpson, Paul Foster, Katherine Baines, Peter Gibson, Ming Yang
2017 Maltby S, Gibson PG, Powell H, Mcdonald VM, 'OMALIZUMAB TREATMENT RESPONSE IN A SEVERE ALLERGIC ASTHMA POPULATION WITH OVERLAPPING COPD', RESPIROLOGY (2017)
Co-authors Vanessa Mcdonald, Peter Gibson
2017 Plank MW, Kaiko GE, Maltby S, Weaver J, Tay H, Shen W, et al., 'TH22 CELLS FORM A DISTINCT TH LINEAGE FROM TH17 CELLS IN VITRO WITH UNIQUE TRANSCRIPTIONAL PROPERTIES AND TBET-DEPENDENT TH1 PLASTICITY DURING INFLUENZA INFECTION IN VIVO', RESPIROLOGY (2017)
Co-authors Gerard Kaiko, 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 Ming Yang, 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 Alan Hsu, Nathan Bartlett, Philip Hansbro, Ming Yang
2016 Maltby S, Lochrin A, Donges B, Tay H, Plank M, Stewart J, Foster P, 'Virus infections impact structural bone cell populations', EUROPEAN JOURNAL OF IMMUNOLOGY, Melbourne, AUSTRALIA (2016)
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 Jodie Simpson, Paul Foster, Ming Yang, Peter Gibson
2015 Plank M, Kaiko G, Maltby S, Tay H, Stewart J, Durum S, Foster P, 'Mapping the cellular source and role of IL-22 in murine lung infections', EUROPEAN RESPIRATORY JOURNAL (2015)
DOI 10.1183/13993003.congress-2015.PA2616
Co-authors Paul Foster
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 Joerg Mattes, Gerard Kaiko, Ming Yang, Philip Hansbro, Paul Foster, Hock Tay
2015 Mateer S, Marks E, Maltby S, Goggins B, Horvat J, Hansbro P, Keely S, 'Pulmonary retention of PMN attracts primed intestinal lymphocytes in a mouse model of inflammatory bowel disease', FASEB JOURNAL (2015) [E3]
Co-authors Bridie Goggins, Jay Horvat, Simon Keely, Philip Hansbro
2014 Mateer S, Maltby S, Marks E, Goggins B, Horvat J, Hansbro P, Keely S, 'Immune cell mis-homing drives secondary organ inflammation in inflammatory bowel disease; a focus on the respiratory system', JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY (2014) [E3]
Co-authors Jay Horvat, Philip Hansbro, Simon Keely, Bridie Goggins
2012 McNagny K, Debruin E, Gold M, Bennett J, Blanchet M-R, Maltby S, Hughes M, 'CD34 family proteins are key regulators of inflammatory cell migration and vascular integrity', JOURNAL OF IMMUNOLOGY, Boston, MA (2012) [E3]
Citations Web of Science - 1
2011 Maltby S, Gold M, Wohlfarth C, Blanchet M, McNagny KM, 'CD34 LOCALIZATION IN EOSINOPHILS AT STEADY STATE AND DURING DISEASE', EXPERIMENTAL HEMATOLOGY (2011) [E3]
2008 Blanchet M-R, Maltby S, Bennett J, McNagny K, 'Mouse models to study the role of CD34 in allergy and inflammatory diseases', FASEB JOURNAL (2008) [E3]
2007 Hughes MR, Anderson N, Maltby S, Wong J, Milenkovic Z, Wang C, et al., 'A new model of hereditary spherocytosis demonstrates profound homeostatic compensation in severely anemic mice.', BLOOD, Atlanta, GA (2007)
2007 Hughes MR, Maltby S, Zbytnuik L, Paulson R, McNagny KM, 'Podocalyxin is a selective marker of erythroid progenitors but is dispensable for anemia recovery.', BLOOD, Atlanta, GA (2007)
Show 15 more conferences
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Grants and Funding

Summary

Number of grants 10
Total funding $608,400

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


20161 grants / $22,500

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 Investigator
Funding Start 2016
Funding Finish 2016
GNo G1600577
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20151 grants / $1,500

Keystone Symposium: Hematopoiesis, Colorado USA, 22-27 February 2015$1,500

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

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Steven Maltby
Scheme Travel Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1500324
Type Of Funding Internal
Category INTE
UON Y

20143 grants / $44,216

Miltenyi Biotec GentleMACS Octo Dissociator with Heaters $23,566

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Phil Hansbro, Laureate Professor Paul Foster, Professor Darryl Knight, Professor Dirk Van Helden, Professor Joerg Mattes, Professor Jodie Simpson, Professor Lisa Wood, Professor Liz Milward, Dr NATHAN Bartlett, Associate Professor Simon Keely, Doctor Steven Maltby, Doctor Andrew Jarnicki, Doctor Malcolm Starkey, Doctor Adam Collison, Doctor Shaan Gellatly
Scheme Equipment Grant
Role Investigator
Funding Start 2014
Funding Finish 2014
GNo G1500861
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

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 Lead
Funding Start 2014
Funding Finish 2014
GNo G1401394
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Inaugural Future of Experimental Medicine Conference: Inflammation in Disease and Ageing, Sydney Australia, 16-19 March 2014$650

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

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Steven Maltby
Scheme Travel Grant
Role Lead
Funding Start 2014
Funding Finish 2014
GNo G1400166
Type Of Funding Internal
Category INTE
UON Y

20132 grants / $21,500

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, Associate 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

43rd Annual Scientific meeting of the Australasian Society for Immunology (ASI), Wellington New Zealand, 2 - 5 December 2013$1,500

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

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Steven Maltby
Scheme Travel Grant
Role Lead
Funding Start 2013
Funding Finish 2014
GNo G1300439
Type Of Funding Internal
Category INTE
UON Y

20123 grants / $518,684

2011 Research Fellowship - DVCR Strategic Appointment (PRCARD)$348,315

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Doctor Steven Maltby
Scheme Research Fellowship
Role Lead
Funding Start 2012
Funding Finish 2015
GNo G1100534
Type Of Funding Internal
Category INTE
UON Y

Post-Doctoral Research Fellowship$150,000

Funding body: Canadian Institutes of Health Research (CIHR)

Funding body Canadian Institutes of Health Research (CIHR)
Scheme Health Research
Role Lead
Funding Start 2012
Funding Finish 2015
GNo
Type Of Funding International - Competitive
Category 3IFA
UON N

Fellowship Start-up Grant$20,369

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Doctor Steven Maltby
Scheme Fellowship Grant
Role Lead
Funding Start 2012
Funding Finish 2012
GNo G1200114
Type Of Funding Internal
Category INTE
UON Y
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Research Supervision

Number of supervisions

Completed3
Current0

Past Supervision

Year Level of Study Research Title Program Supervisor Type
2017 PhD Modeling of Respiratory Syncytial Virus-induced Exacerbation of Allergic Airways Disease PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2017 PhD Understanding the Mechanisms of Bacterial-Induced Exacerbation of Allergic Airways Disease in a Mouse Model PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2016 Honours The Systemic Impacts of Viral Inflammation on the Structural Integrity of Bone and Haematopoiesis Medical Science, The University of Newcastle - Faculty of Health and Medicine Co-Supervisor
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Dr Steven Maltby

Positions

Research Academic
School of Nursing and Midwifery
Faculty of Health and Medicine

Project Officer
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Casual Academic
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Casual Research Assistant
School of Medicine and Public Health
Faculty of Health and Medicine

Contact Details

Email steven.maltby@newcastle.edu.au
Phone (02) 404 20173
Links Research Networks
Twitter
Research Networks

Office

Room MSB 317
Building MS Building
Location NEWCASTLE

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