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Dr Steven Maltby

Postdoctoral Research Fellow

School of Biomedical Sciences and Pharmacy

Down to the Marrow

Dr Steven Maltby is interested in the body’s response to infection and inflammation, with dual focusses on severe asthma, and the role of bone marrow in immune responses.

Dr Steven Maltby

When it is working well, we don’t even notice it. But when the body’s immune system is improperly activated it leads to chronic disease, including asthma and osteoporosis.

Steven is looking at the mechanisms that shape the bone marrow response in the hope of magnifying the good and eliminating the bad.

Dividing his time between two roles, Steven spends three days a week as a Research Academic at the Centre of Research Excellence (CRE) in Severe Asthma.

Steven dedicates his time to communicating research results, translation of knowledge into practice, as well as Centre logistics.

For two days a week, he works as a Post-doctoral Research Fellow, with Laureate Professor Paul Foster’s research group.

“A lot of the focus in our lab is on asthma and exacerbations of asthma,” Steven explains.

“I look at viral infections because they worsen asthma, and whether any of that worsening is through bone marrow changes is an open question.”

Following function

Bone marrow, the soft tissue in the middle of your long bones, is the site of production of immune cells and blood cells, as well as cells that create bone itself.

Steven’s research sees him positioned in a relatively unique space.

“My work studying bone marrow cells sits at the junction of immunology, and the study of bones,” Steven explains.

“From the development side of things people study these cells making bone. From the immune side, people study these cells in their role of regulating stem cell space.”

“I am interested in how and why the marrow creates different cell types, and the mechanisms behind that.”

Steven points out that there has been a massive change in our understanding of bone marrow function in the last fifteen years.

“We believed that bone marrow was nicely isolated from most infections and inflammation and just kept ticking over, making new bone cells and immune cells everyday,” he says.

“Now there is more recognition that signals produced during infection go all the way back to the bone marrow, and actually change production and maybe the function of those cells.”

Bones of contention

“We are interested in looking at the responses in the bone marrow to short-term infections with a virus, and long-term inflammation with a disease such as asthma.”

During a virus infection, an immune response is required to kill the virus and infected cells.

“If you get a really bad infection, you actually get signals and communication back from the site of infection that change the production of immune cells,” Steven notes.

“You get signals back to the bone marrow that say look, we are not taking care of this, we need to increase the production of immune cells.”

“On the other side, we are finding that if you get that infection you also reduce the cells responsible for making bone.”

The bone marrow putting bone production on-hold production to focus on creating cells designed to defeat a infection makes sense in the short term, but what about the long term?

Too much of a good thing

Problems occur when the body’s defense system becomes confused or hyper-vigilant.

“In cases of chronic inflammation in diseases such as arthritis, inflammatory bowel disease, and asthma, the bone marrow seems to interpret this inflammation as infection,” Steven says.

“Whereas your immune response might be really positive when you want to deal with the flu in a week, it is really negative when you have got it going on constantly for 20 years of your life.”

“You are constantly making extra immune cells which make the inflammation worse, and taking energy away from making bone.”

Using model systems, Steven is trying to understand the basic molecular mechanisms related to different features of disease, in the hope of reversing harmful effects.

“If we understand the mechanisms we can develop drugs that target different parts of that pathway, or are upstream at beginning of the pathway. Or even find a master regulator that blocks the entire process altogether.”

New hope

Educating the public and healthcare practitioners regarding new medications that target specific pathways related to severe asthma is part of Steven’s role at the CRE in Severe Asthma.

A network of clinicians and researchers focused on severe asthma, the CRE has a clinical focus, prioritizing the translation of research outcomes into practice.

“Looking at patient samples is important, but looking at how you treat and manage severe asthma, and developing better mechanisms to handle it in the healthcare system are equally important,” Steven says.

Despite the common belief that asthma can be easily controlled by preventative medication, one percent of Australians have a form of asthma that does not respond to widely used treatments.

“We are still amongst the highest in the developed world for asthma deaths. People are still dying of asthma.”

Steven explains that new medications have provided hope for these extreme cases of treatment-refractory asthma.

Eosinophils are a type of white blood cell produced by the immune system that are involved in allergies, asthma, and defense against parasites.

One therapy reduces eosinophil production in severe asthmatics to normal levels, alleviating and repairing symptoms - such as inflammation of the airways.

Another new medication, anti-immunoglobulin E therapy, works by interfering with the development of allergic inflammation.

Knowledge into practice

Although excited by the potential of these new medications to relieve discomfort and symptoms for severe asthmatics, Steven is quick to point out that the specificity of these therapies mean they will not work for all patients.

The first step in introducing these new medications is to develop consensus on the process of assessing individual patients to see if the targeted pathways are important for their individual disease.

Future steps will be necessary with the availability of multiple therapies, requiring consensus on how to choose one drug over another.

“For some patients, biomarkers will be clear indicators of whether one or the other new therapy is likely to work,” says Steven.

“The tricky thing will be choosing one medication, when multiple options seem suitable in some patients.”

“We need discussion and consensus to get the best outcomes for people who have been living their lives with severe asthma.”

This research will continue to explore and target asthma, as well as other diseases caused by cell changes in the bone marrow.

“The idea is to work out the mechanisms, to identify what part of the process and what molecules are causing the changes.”

“Using model systems, we need to go in there and tinker with the different parts, and see what effect we have.”

“Then based on that data then we will get an understanding of what is good and what is bad and expand it from there.”

Down to the Marrow

Steven's research is focussed on characterizing changes in the bone marrow during disease and infection.

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Career Summary

Biography

I currently work 3 days/week with the Centre of Excellence in Severe Asthma (www.severeasthma.org.au). In my role as a Research Academic, I am actively involved in science communications and logistics and administration of the research network.

My remaining 2 days/week, I work as a Post-doctoral Research Fellow, with Laureate Professor Paul Foster's research group. My current research is focussed 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 our studies is to 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. Our second aim is to identify key molecules involved in feedback from sites of infection/inflammation to the bone marrow and the impacts of blocking these molecules on disease pathology.

Past Experience:

I completed my 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 MicroRNA Regulation Immune Cell Activation and Migration Virus Infections

Teaching Expertise
Immunology


Qualifications

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

Keywords

  • Asthma
  • Bone Biology
  • Bone Marrow
  • Disease Models
  • Hematopoiesis
  • Immunology
  • Infection
  • Virus

Languages

  • English (Fluent)

Fields of Research

Code Description Percentage
110309 Infectious Diseases 30
110316 Pathology (excl. Oral Pathology) 20
110799 Immunology not elsewhere classified 50

Professional Experience

UON Appointment

Title Organisation / Department
Postdoctoral Research Fellow

Post-doctoral Research Fellow

University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia
Research Academic

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

University of Newcastle
School of Medicine and Public Health
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 (2 outputs)

Year Citation Altmetrics Link
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 - 4
Co-authors Paul Foster, Joerg Mattes
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

Journal article (16 outputs)

Year Citation Altmetrics Link
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 - 1Web of Science - 1
Co-authors Ming Yang, Peter Gibson, Katherine Baines, Paul Foster, Jodie Simpson
2016 Maltby S, Gibson PG, Powell H, McDonald VM, 'Omalizumab Treatment Response in a Severe Allergic Asthma Population with Overlapping COPD.', Chest, (2016)
DOI 10.1016/j.chest.2016.09.035
Co-authors Peter Gibson, Vanessa Mcdonald
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)
DOI 10.1371/journal.pone.0163392
Co-authors Ming Yang, Paul Foster
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, 98 727-737 (2015) [C1]
DOI 10.1189/jlb.3RU1114-563R
Citations Scopus - 1Web of Science - 1
Co-authors Jay Horvat, Paul Foster, Philip Hansbro, Simon Keely
2015 Tay HL, Kaiko GE, Plank M, Li J, Maltby S, Essilfie AT, 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]
Citations Scopus - 3
Co-authors Philip Hansbro, Paul Foster, Ming Yang, 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]

© 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. Level... [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 - 15Web of Science - 15
Co-authors Paul Foster, Ming Yang, Joerg Mattes
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 - 2Web of Science - 1
Co-authors Philip Hansbro, 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 - 5Web of Science - 8
Co-authors Joerg Mattes, Paul Foster, Philip Hansbro, 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 - 4Web of Science - 2
Co-authors Paul Foster, Nicole Hansbro
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 (2011) [C1]
DOI 10.1371/journal.pone.0018160
Citations Scopus - 13Web of Science - 10
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 - 22Web of Science - 19
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 - 16Web of Science - 18
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 - 14Web of Science - 11
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 - 4Web of Science - 4
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 - 44Web of Science - 43
Show 13 more journal articles

Review (6 outputs)

Year Citation Altmetrics Link
2016 Maltby S, Plank M, Tay HL, Collison A, Foster PS, 'Targeting MicroRNA Function in Respiratory Diseases: Mini-Review.', Front Physiol (2016)
DOI 10.3389/fphys.2016.00021
Citations Scopus - 3Web of Science - 2
Co-authors Adam Collison, Paul Foster
2016 Wark PA, Hew M, Maltby S, McDonald VM, Gibson PG, 'Diagnosis and investigation in the severe asthma clinic.', Expert Rev Respir Med (2016)
DOI 10.1586/17476348.2016.1165096
Co-authors Peter Gibson, Peter Wark, Vanessa Mcdonald
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)

© 2016 Informa UK Limited, trading as Taylor & Francis Group.Severe asthma is a complex multifactorial disease that requires specialist multidisciplinary input for optimal clinic... [more]

© 2016 Informa UK Limited, trading as Taylor & Francis Group.Severe asthma is a complex multifactorial disease that requires specialist multidisciplinary input for optimal clinical outcomes. Following multidimensional assessment for optimisation of current therapy, self-management skills and comorbidities, all patients should be accurately phenotyped. Only after this assessment has been completed should new monoclonal antibody therapies be considered. In this review, we summarise the new antibody approaches targeting identified pathological pathways in severe refractory asthma.

DOI 10.1586/17512433.2016.1172208
Co-authors Peter Wark, Vanessa Mcdonald, Peter Gibson, Christopher Grainge
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 (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 - 22Web of Science - 20
Co-authors Joerg Mattes, 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 (2013) [C1]
DOI 10.1111/cea.12170
Co-authors Paul Foster, Joerg Mattes
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 - 140Web of Science - 119
Show 3 more reviews

Conference (12 outputs)

Year Citation Altmetrics Link
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 (2016)
Co-authors Alan Hsu, 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 (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 (2016)
Co-authors Ming Yang, Jodie Simpson, 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 (2015) [E3]
Co-authors Ming Yang, Paul Foster, Philip Hansbro, Joerg Mattes
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 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 Simon Keely, Philip Hansbro, Jay Horvat
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 (2012) [E3]
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 (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 (2007)
Show 9 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, Associate Professor Jodie Simpson, Associate Professor Lisa Wood, Associate Professor Liz Milward, Dr NATHAN Bartlett, Doctor 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, Associate Professor Jodie Simpson, Professor Rakesh Kumar, Doctor Nicole Hansbro, Doctor Steven Maltby, Doctor Ming Yang, Doctor Gerard Kaiko, Doctor Jay Horvat, Doctor 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

Completed1
Current2

Total current UON EFTSL

PhD0.4

Current Supervision

Commenced Level of Study Research Title / Program / Supervisor Type
2012 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
2012 PhD Understanding the mechanisms of airway hyper-responsiveness in a mouse model of asthma
PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle
Co-Supervisor

Past Supervision

Year Level of Study Research Title / Program / Supervisor Type
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

Postdoctoral Research Fellow
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Research Academic
School of Medicine and Public Health
Faculty of Health and Medicine

Contact Details

Email steven.maltby@newcastle.edu.au
Phone (02) 404 20173
Fax (02) 404 20025
Links Research Networks
Twitter

Office

Room HMRI Level 2
Building HMRI
Location NEWCASTLE

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