Dr Jemma Mayall

Dr Jemma Mayall

Post Doctoral Researcher

School of Biomedical Sciences and Pharmacy

Career Summary

Biography

Dr. Jemma Mayall is a postdoctoral researcher in the Viruses, Infections/Immunity, Vaccines and Asthma research group at the Hunter Medical Research Institute (HMRI). Dr. Mayall's research investigates the role of innate immune responses in infections of the respiratory and reproductive tracts to determine how these responses can be manipulated to prevent and treat associated diseases. 

Infections of the female reproductive tract frequently lead to chronic diseases such as pelvic inflammatory disease, chronic pelvic pain and infertility. Often, these infections aren't diagnosed until it's too late to prevent permanent immunopathology due to their asymptomatic nature, as is the case with Chlamydia. Chlamydia infections damage the reproductive organs by triggering prolonged inflammatory responses mediated by the innate immune system.

Similarly, most infections of the respiratory tract cause disease by inducing inflammatory responses in the lung, and in severe cases, systemically. Influenza infections trigger a cytokine storm in the lung that can be fatal. The mutation rate of viruses like influenza means that current vaccines and antiviral therapies are doomed to become ineffective. 

However, some innate immune processes are effective at protecting against and clearing infections of the respiratory and reproductive tracts. Dr. Mayall's research aims to determine which of these innate responses are protective, and which contribute to the development of pathology, in order to identify new targets for preventing and treating infection and inflammation-associated diseases.

Dr. Mayall's research has identified novel mechanisms of inflammatory diseases of both the respiratory and reproductive tracts and, by investigating newly discovered innate immune factors and signalling pathways, she has shown how manipulating the expression of these can boost protective responses and reduce infection and inflammation.


Qualifications

  • Doctor of Philosophy, University of Newcastle
  • Bachelor of Biomedical Sciences, University of Newcastle
  • Bachelor of Biomedical Sciences (Hons), University of Newcastle

Keywords

  • Immunology
  • Innate immunity
  • Microbiology
  • Mucosal immunology
  • Respiratory infections
  • Sexually transmitted infections

Languages

  • English (Mother)

Fields of Research

Code Description Percentage
110309 Infectious Diseases 40
110899 Medical Microbiology not elsewhere classified 10
110707 Innate Immunity 50

Professional Experience

UON Appointment

Title Organisation / Department
Post Doctoral Researcher University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia

Awards

Award

Year Award
2016 ICI Travel Award
Australasian Society for Immunology
2015 ASI Travel Award
Australasian Society for Immunology

Invitations

Speaker

Year Title / Rationale
2019 Love is a battlefield: the war against Chlamydia

Teaching

Code Course Role Duration
HUBS2505 Human Pathophysiology
School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle
Lecturer 29/4/2019 - 30/4/2019
HUBS3602 Human Infection and Immunity 2
School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle
Lecturer 12/3/2018 - 10/3/2020
HUBS3602 Human Infection and Immunity 2
School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle
Laboratory demonstrator 6/4/2011 - 11/5/2016
HUBS2601 Human infection & Immunity I
School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle
Laboratory demonstrator and tutor 6/4/2011 - 14/5/2014
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Publications

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


Journal article (10 outputs)

Year Citation Altmetrics Link
2020 Ali MK, Kim RY, Brown AC, Donovan C, Vanka KS, Mayall JR, et al., 'Critical role for iron accumulation in the pathogenesis of fibrotic lung disease.', J Pathol, 251 49-62 (2020)
DOI 10.1002/path.5401
Citations Scopus - 2Web of Science - 1
Co-authors Philip Hansbro, Chantal Donovan, Jay Horvat, Liz Milward
2020 Lee JM, Mayall JR, Chevalier A, McCarthy H, Van Helden D, Hansbro PM, et al., 'Chlamydia muridarum infection differentially alters smooth muscle function in mouse uterine horn and cervix.', Am J Physiol Endocrinol Metab, 318 E981-E994 (2020)
DOI 10.1152/ajpendo.00513.2019
Co-authors Dirk Vanhelden, Philip Hansbro, Jay Horvat, Phillip Jobling
2020 Ali MK, Kim RY, Brown AC, Mayall JR, Karim R, Pinkerton JW, et al., 'Crucial role for lung iron level and regulation in the pathogenesis and severity of asthma.', Eur Respir J, 55 (2020)
DOI 10.1183/13993003.01340-2019
Co-authors Chantal Donovan, Paul Foster, Liz Milward, Liz Holliday, Philip Hansbro, Jay Horvat, Peter Wark, Malcolm Starkey
2018 Stifter SA, Matthews AY, Mangan NE, Fung KY, Drew A, Tate MD, et al., 'Defining the distinct, intrinsic properties of the novel type I interferon, IFN .', The Journal of biological chemistry, 293 3168-3179 (2018) [C1]
DOI 10.1074/jbc.m117.800755
Citations Scopus - 10Web of Science - 9
Co-authors Philip Hansbro
2017 Hansbro PM, Kim RY, Starkey MR, Donovan C, Dua K, Mayall JR, et al., 'Mechanisms and treatments for severe, steroid-resistant allergic airway disease and asthma', Immunological Reviews, 278 41-62 (2017) [C1]

© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd Severe, steroid-resistant asthma is clinically and economically important since affected individuals d... [more]

© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd Severe, steroid-resistant asthma is clinically and economically important since affected individuals do not respond to mainstay corticosteroid treatments for asthma. Patients with this disease experience more frequent exacerbations of asthma, are more likely to be hospitalized, and have a poorer quality of life. Effective therapies are urgently required, however, their development has been hampered by a lack of understanding of the pathological processes that underpin disease. A major obstacle to understanding the processes that drive severe, steroid-resistant asthma is that the several endotypes of the disease have been described that are characterized by different inflammatory and immunological phenotypes. This heterogeneity makes pinpointing processes that drive disease difficult in humans. Clinical studies strongly associate specific respiratory infections with severe, steroid-resistant asthma. In this review, we discuss key findings from our studies where we describe the development of representative experimental models to improve our understanding of the links between infection and severe, steroid-resistant forms of this disease. We also discuss their use in elucidating the mechanisms, and their potential for developing effective therapeutic strategies, for severe, steroid-resistant asthma. Finally, we highlight how the immune mechanisms and therapeutic targets we have identified may be applicable to obesity-or pollution-associated asthma.

DOI 10.1111/imr.12543
Citations Scopus - 38Web of Science - 35
Co-authors Chantal Donovan, Darryl Knight, Jay Horvat, Paul Foster, Philip Hansbro, Malcolm Starkey, Nicole Hansbro, Jodie Simpson, Lisa Wood
2017 Kim RY, Horvat JC, Pinkerton JW, Starkey MR, Essilfie AT, Mayall JR, et al., 'MicroRNA-21 drives severe, steroid-insensitive experimental asthma by amplifying phosphoinositide 3-kinase mediated suppression of histone deacetylase 2', Journal of Allergy and Clinical Immunology, 139 519-532 (2017) [C1]

© 2016 American Academy of Allergy, Asthma & Immunology Background Severe steroid-insensitive asthma is a substantial clinical problem. Effective treatments are urgently req... [more]

© 2016 American Academy of Allergy, Asthma & Immunology Background Severe steroid-insensitive asthma is a substantial clinical problem. Effective treatments are urgently required, however, their development is hampered by a lack of understanding of the mechanisms of disease pathogenesis. Steroid-insensitive asthma is associated with respiratory tract infections and noneosinophilic endotypes, including neutrophilic forms of disease. However, steroid-insensitive patients with eosinophil-enriched inflammation have also been described. The¿mechanisms that underpin infection-induced, severe steroid-insensitive asthma can be elucidated by using mouse models of disease. Objective We sought to develop representative mouse models of severe, steroid-insensitive asthma and to use them to identify pathogenic mechanisms and investigate new treatment approaches. Methods Novel mouse models of Chlamydia, Haemophilus influenzae, influenza, and respiratory syncytial virus respiratory¿tract infections and ovalbumin-induced, severe, steroid-insensitive allergic airway disease (SSIAAD) in BALB/c mice were developed and interrogated. Results Infection induced increases in the levels of microRNA (miRNA)-21 (miR-21) expression in the lung during SSIAAD, whereas expression of the miR-21 target phosphatase and tensin homolog was reduced. This was associated with an increase in levels of phosphorylated Akt, an indicator of phosphoinositide 3-kinase (PI3K) activity, and decreased nuclear histone deacetylase (HDAC)2 levels. Treatment with an miR-21¿specific antagomir (Ant-21) increased phosphatase and tensin homolog levels. Treatment with Ant-21, or the pan-PI3K inhibitor LY294002, reduced PI3K activity and restored HDAC2 levels. This led to suppression of airway hyperresponsiveness and restored steroid sensitivity to allergic airway disease. These observations were replicated with SSIAAD associated with 4 different pathogens. Conclusion We identify a previously unrecognized role for an¿miR-21/PI3K/HDAC2 axis in SSIAAD. Our data highlight miR-21 as a novel therapeutic target for the treatment of this form of asthma.

DOI 10.1016/j.jaci.2016.04.038
Citations Scopus - 67Web of Science - 71
Co-authors Philip Hansbro, Paul Foster, Nicole Hansbro, Simon Keely, Joerg Mattes, Jay Horvat, Malcolm Starkey
2017 Ali MK, Kim RY, Karim R, Mayall JR, Martin KL, Shahandeh A, et al., 'Role of iron in the pathogenesis of respiratory disease', INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 88 181-195 (2017) [C1]
DOI 10.1016/j.biocel.2017.05.003
Citations Scopus - 14Web of Science - 14
Co-authors Liz Milward, Jay Horvat, Philip Hansbro, Malcolm Starkey
2017 Kim RY, Pinkerton JW, Essilfie AT, Robertson AAB, Baines KJ, Brown AC, et al., 'Role for NLRP3 inflammasome-mediated, IL-1ß-dependent responses in severe, steroid-resistant asthma', American Journal of Respiratory and Critical Care Medicine, 196 283-297 (2017) [C1]

© 2017 by the American Thoracic Society. Rationale: Severe, steroid-resistant asthma is the major unmet need in asthma therapy. Disease heterogeneity and poor understanding of pat... [more]

© 2017 by the American Thoracic Society. Rationale: Severe, steroid-resistant asthma is the major unmet need in asthma therapy. Disease heterogeneity and poor understanding of pathogenic mechanisms hampers the identification of therapeutic targets. Excessive nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome and concomitant IL-1ß responses occur in chronic obstructive pulmonary disease, respiratory infections, and neutrophilic asthma. However, the direct contributions to pathogenesis, mechanisms involved, and potential for therapeutic targeting remain poorly understood, and are unknown in severe, steroid-resistant asthma. Objectives: To investigate the roles and therapeutic targeting of the NLRP3 inflammasome and IL-1ß in severe, steroid-resistant asthma. Methods: We developed mouse models of Chlamydia and Haemophilus respiratory infection-mediated, ovalbumin-induced severe, steroid-resistant allergic airway disease. These models share the hallmark features of human disease, including elevated airway neutrophils, and NLRP3 inflammasome and IL-1ß responses. The roles and potential for targeting of NLRP3 inflammasome, caspase-1, and IL-1ß responses in experimental severe, steroid-resistant asthma were examined using a highly selective NLRP3 inhibitor, MCC950; the specific caspase-1 inhibitor Ac-YVAD-cho; and neutralizing anti-IL-1ß antibody. Roles for IL-1ß-induced neutrophilic inflammation were examined using IL-1ß and anti-Ly6G. Measurements and Main Results: Chlamydia and Haemophilus infections increase NLRP3, caspase-1, IL-1ß responses that drive steroid-resistant neutrophilic inflammation and airway hyperresponsiveness. Neutrophilic airway inflammation, disease severity, and steroid resistance in human asthma correlate with NLRP3 and IL-1ß expression. Treatment with anti-IL-1ß, Ac- YVAD-cho, and MCC950 suppressed IL-1ß responses and the important steroid-resistant features of disease in mice, whereas IL-1ß administration recapitulated these features. Neutrophil depletion suppressed IL-1ß-induced steroid-resistant airway hyperresponsiveness. Conclusions: NLRP3 inflammasome responses drive experimental severe, steroid-resistant asthma and are potential therapeutic targets in this disease.

DOI 10.1164/rccm.201609-1830OC
Citations Scopus - 96Web of Science - 94
Co-authors Peter Gibson, Peter Wark, Malcolm Starkey, Lisa Wood, Jay Horvat, Darryl Knight, Jodie Simpson, Philip Hansbro, Katherine Baines, Nicole Hansbro
2015 Essilfie A, Horvat JC, Kim RY, Mayall JR, Pinkerton JW, Beckett EL, et al., 'Macrolide therapy suppresses key features of experimental steroid-sensitive and steroid-insensitive asthma', Thorax Journal, 70 458-467 (2015) [C1]
DOI 10.1136/thoraxjnl-2014-206067
Citations Scopus - 64Web of Science - 68
Co-authors Paul Foster, Jodie Simpson, Emma Beckett, Jay Horvat, Malcolm Starkey, Philip Hansbro, Peter Gibson
2013 Fung KY, Mangan NE, Cumming H, Horvat JC, Mayall JR, Stifter SA, et al., 'Interferon-epsilon Protects the Female Reproductive Tract from Viral and Bacterial Infection', SCIENCE, 339 1088-1092 (2013) [C1]
DOI 10.1126/science.1233321
Citations Scopus - 118Web of Science - 116
Co-authors Jay Horvat, John Schjenken, Philip Hansbro
Show 7 more journal articles

Conference (7 outputs)

Year Citation Altmetrics Link
2019 Kim R, Horvat J, Pinkerton J, Rae B, Brown A, Hsu A, et al., 'INTERRELATIONSHIP BETWEEN MICRORNA-21, IL-1 beta AND SLC26A4 RESPONSES IN SEVERE ASTHMA', RESPIROLOGY (2019)
Co-authors Bridie Goggins, Malcolm Starkey, Philip Hansbro, Alan Hsu, Peter Wark, Jay Horvat
2017 Horvat JC, Ali MK, Johnstone D, Kim RY, Mayall JR, Karim R, et al., 'Role for dysregulated iron in the pathogenesis of murine models of lung disease', Washington, DC (2017)
Co-authors Jay Horvat, Liz Milward, Philip Hansbro
2015 Kim R, Horvat J, Pinkerton J, Starkey M, Essilfie A, Mayall J, et al., 'INFECTION-INDUCED MICRORNA-21 DRIVES SEVERE, STEROID-INSENSITIVE EXPERIMENTAL ASTHMA BY AMPLIFYING PI3K-MEDIATED SUPPRESSION OF HDAC2', RESPIROLOGY, Queensland, AUSTRALIA (2015) [E3]
Co-authors Jay Horvat, Malcolm Starkey, Philip Hansbro, Simon Keely, Paul Foster, Joerg Mattes
2014 Horvat J, Kim R, Mayall J, Pinkerton J, Starkey M, Essilfie A, et al., 'ANTIOXIDANT-BASED THERAPY FOR THE SUPPRESSION OF EARLY- LIFE INFECTION-INDUCED SEVERE ASTHMA', RESPIROLOGY (2014) [E3]
DOI 10.1111/resp.12263_2
Co-authors Philip Hansbro, Malcolm Starkey, Jay Horvat, Lisa Wood
2013 Hansbro P, Horvat J, Essilfie A-T, Kim R, Mayall J, Starkey M, Foster P, 'Macrolides suppress key features of experimental steroid-sensitive and steroid-resistant asthma', JOURNAL OF IMMUNOLOGY, Honolulu, HI (2013) [E3]
Co-authors Paul Foster, Philip Hansbro, Malcolm Starkey, Emma Beckett, Jay Horvat
2013 Horvat JC, Essilfie A-T, Kim RY, Mayall JR, Starkey MR, Beckett EL, et al., 'MACROLIDES SUPPRESS KEY FEATURES OF EXPERIMENTAL STEROID-SENSITIVE AND STEROID-RESISTANT ASTHMA', RESPIROLOGY (2013) [E3]
Co-authors Emma Beckett, Malcolm Starkey, Philip Hansbro, Peter Gibson, Jodie Simpson, Paul Foster, Jay Horvat
2012 Horvat JC, Essilfie A-T, Kim RY, Mayall JR, Starkey MR, Beckett EL, et al., 'Efficacy of antibiotic-based therapeutic strategies for the treatment of infection-induced, steroid-resistant allergic airways disease', Respirology, Canberra, ACT (2012) [E3]
Co-authors Paul Foster, Philip Hansbro, Emma Beckett, Jay Horvat, Malcolm Starkey
Show 4 more conferences
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Grants and Funding

Summary

Number of grants 3
Total funding $20,750

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


20201 grants / $4,550

Understanding the link between reproductive tract inflammation and chronic pelvic pain$4,550

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

Funding body Faculty of Health and Medicine, University of Newcastle
Project Team

A/Prof Phil Jobling, A/Prof Jay Horvat

Scheme Faculty of Health and Medicine Strategic Research Pilot Grant
Role Lead
Funding Start 2020
Funding Finish 2020
GNo
Type Of Funding Internal
Category INTE
UON N

20191 grants / $6,200

The University of Newcastle FHEAM International Research Visiting Fellowship $6,200

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

Funding body Faculty of Health and Medicine, University of Newcastle
Scheme International Research Visiting Fellowship
Role Lead
Funding Start 2019
Funding Finish 2019
GNo
Type Of Funding Internal
Category INTE
UON N

20171 grants / $10,000

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
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Research Supervision

Number of supervisions

Completed0
Current3

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2020 PhD The Role and Therapeutic Targeting of IFN¿ in Viral Exacerbations of Asthma and COPD PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2018 PhD Investigating the Role of Inflammasomes in Female Reproductive Tract (FRT) Infections and Associated Disease PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2015 PhD Characterization of physiological and neuronal alterations in Chlamydia reproductive tract infection PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
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Research Projects

Role of IFN-epsilon in infection 2011 -


Infection, inflammation and pelvic pain 2017 -


Innate immune pathways in reproductive and respiratory tract infections 2011 -


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Dr Jemma Mayall

Position

Post Doctoral Researcher
Horvat
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Contact Details

Email jemma.mayall@newcastle.edu.au
Phone (02) 4042 0221

Office

Room HMRI Building Lvl 2E Rm 2413 W2-122
Building HMRI Building
Location John Hunter Hospital Campus

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