Dr Jemma Mayall
Lecturer
School of Biomedical Sciences and Pharmacy
- Email:jemma.mayall@newcastle.edu.au
- Phone:(02) 4042 0221
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 |
---|---|---|
320404 | Cellular immunology | 30 |
320407 | Innate immunity | 50 |
320211 | Infectious diseases | 20 |
Professional Experience
UON Appointment
Title | Organisation / Department |
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Lecturer | University of Newcastle School of Biomedical Sciences and Pharmacy Australia |
Awards
Award
Year | Award |
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2016 |
ICI Travel Award Australasian Society for Immunology |
2015 |
ASI Travel Award Australasian Society for Immunology |
Invitations
Speaker
Year | Title / Rationale |
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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 |
Publications
For publications that are currently unpublished or in-press, details are shown in italics.
Journal article (19 outputs)
Year | Citation | Altmetrics | Link | ||||||||
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2024 |
Mayall JR, Horvat JC, Mangan NE, Chevalier A, McCarthy H, Hampsey D, et al., 'Interferon-epsilon is a novel regulator of NK cell responses in the uterus', EMBO Molecular Medicine, 16 267-293 [C1]
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2023 |
'TSANZ Abstracts', Respirology, 28 28-109 (2023)
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2023 |
'The 27th Congress of the Asian Pacific Society of Respirology, 16-19 November 2023, Singapore.', Respirology, 28 Suppl 4 3-425 (2023) [C1]
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2023 |
Horvat JC, Kim RY, Weaver N, Augood C, Brown AC, Donovan C, et al., 'Characterization and inhibition of inflammasome responses in severe and non-severe asthma.', Respir Res, 24 303 (2023) [C1]
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2023 |
Cooper GE, Mayall J, Donovan C, Haw TJ, Budden KF, Hansbro NG, et al., 'Antiviral Responses of Tissue-resident CD49a+ Lung Natural Killer Cells Are Dysregulated in Chronic Obstructive Pulmonary Disease.', Am J Respir Crit Care Med, 207 553-565 (2023) [C1]
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Nova | |||||||||
2022 |
Pinkerton JW, Kim RY, Brown AC, Rae BE, Donovan C, Mayall JR, et al., 'Relationship between type 2 cytokine and inflammasome responses in obesity-associated asthma', JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 149 1270-1280 (2022) [C1]
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Nova | |||||||||
2022 |
Donovan C, Kim RY, Galvao I, Jarnicki AG, Brown AC, Jones-Freeman B, et al., 'Aim2 suppresses cigarette smoke-induced neutrophil recruitment, neutrophil caspase-1 activation and anti-Ly6G-mediated neutrophil depletion', IMMUNOLOGY AND CELL BIOLOGY, 100 235-249 (2022) [C1]
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Nova | |||||||||
2021 |
Barnes JL, Plank MW, Asquith K, Maltby S, Sabino LR, Kaiko GE, et al., 'T-helper 22 cells develop as a distinct lineage from Th17 cells during bacterial infection and phenotypic stability is regulated by T-bet', MUCOSAL IMMUNOLOGY, 14 1077-1087 (2021) [C1]
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Nova | |||||||||
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', American Journal of Physiology - Endocrinology and Metabolism, 318 E981-E994 (2020) [C1] Lee JM, Mayall JR, Chevalier A, McCarthy H, Van Helden D, Hansbro PM, Horvat JC, Jobling P. Chlamydia muridarum infection differentially alters smooth muscle function in mouse ute... [more] Lee JM, Mayall JR, Chevalier A, McCarthy H, Van Helden D, Hansbro PM, Horvat JC, Jobling P. Chlamydia muridarum infection differentially alters smooth muscle function in mouse uterine horn and cervix. Am J Physiol Endocrinol Metab 318: E981 E994, 2020. First published April 21, 2020; doi:10.1152/ajpendo.00513. 2019. Chlamydia trachomatis infection is a primary cause of reproductive tract diseases including infertility. Previous studies showed that this infection alters physiological activities in mouse oviducts. Whether this occurs in the uterus and cervix has never been investigated. This study characterized the physiological activities of the uterine horn and the cervix in a Chlamydia muridarum (Cmu)-infected mouse model at three infection time points of 7, 14, and 21 days postinfection (dpi). Cmu infection significantly decreased contractile force of spontaneous contraction in the cervix (7 and 14 dpi; P < 0.001 and P < 0.05, respectively), but this effect was not observed in the uterine horn. The responses of the uterine horn and cervix to oxytocin were significantly altered by Cmu infection at 7 dpi (P < 0.0001), but such responses were attenuated at 14 and 21 dpi. Cmu infection increased contractile force to prostaglandin (PGF2_) by 53 83% in the uterine horn. This corresponded with the increased messenger ribonucleic acid (mRNA) expression of Ptgfr that encodes for its receptor. However, Cmu infection did not affect contractions of the uterine horn and cervix to PGE2 and histamine. The mRNA expression of Otr and Ptger4 was inversely correlated with the mRNA expression of Il1b, Il6 in the uterine horn of Cmu-inoculated mice (P < 0.01 to P < 0.001), suggesting that the changes in the Otr and Ptger4 mRNA expression might be linked to the changes in inflammatory cytokines. Lastly, this study also showed a novel physiological finding of the differential response to PGE2 in mouse uterine horn and cervix.
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Nova | |||||||||
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', JOURNAL OF PATHOLOGY, 251 49-62 (2020) [C1]
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Nova | |||||||||
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', EUROPEAN RESPIRATORY JOURNAL, 55 (2020) [C1]
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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]
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Nova | |||||||||
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] Severe, steroid-resistant asthma is clinically and economically important since affected individuals do not respond to mainstay corticosteroid treatments for asthma. Patients with... [more] 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.
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Nova | |||||||||
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] Background Severe steroid-insensitive asthma is a substantial clinical problem. Effective treatments are urgently required, however, their development is hampered by a lack of und... [more] 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.
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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]
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Nova | |||||||||
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] Rationale: Severe, steroid-resistant asthma is the major unmet need in asthma therapy. Disease heterogeneity and poor understanding of pathogenic mechanisms hampers the identifica... [more] 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.
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2016 |
'Abstracts of ICI 2016 International Congress of Immunology, 21-26 August 2016, Melbourne, Australia.', Eur J Immunol, 46 Suppl 1 1-1238 (2016)
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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]
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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]
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Nova | |||||||||
Show 16 more journal articles |
Conference (17 outputs)
Year | Citation | Altmetrics | Link | |||||
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2023 |
Barnes J, Plank M, Asquith K, Maltby S, Rodrigues SL, Kaiko G, et al., 'T-helper-22 cells develop independently of Th17 cells during bacterial infection', RESPIROLOGY (2023)
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2023 |
Mayall J, Pillar A, Daly K, Brown A, Essilfie A-T, Gomez H, et al., 'LSC-2023-Iron metabolism determines the outcome of influenza A virus infection', EUROPEAN RESPIRATORY JOURNAL, IA, Milan (2023)
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2023 |
Mayall J, Cooper G, Donovan C, Haw T, Budden K, Blomme E, et al., 'Anti-viral responses of tissue-resident NK cells are dysregulated in COPD', Christchurch, New Zealand (2023)
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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]
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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]
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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]
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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]
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Show 14 more conferences |
Preprint (2 outputs)
Year | Citation | Altmetrics | Link | |||||
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2020 |
Hsu AC-Y, Wang G, Reid A, Veerati PC, Pathinayake P, Daly K, et al., 'SARS-CoV-2 Spike protein promotes hyper-inflammatory response that can be ameliorated by Spike-antagonistic peptide and FDA-approved ER stress and MAP kinase inhibitors
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2018 |
Lee JM, Mayall J, Chevalier A, Helden DV, Horvat J, Hansbro P, Jobling P, '
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Grants and Funding
Summary
Number of grants | 10 |
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Total funding | $1,344,731 |
Click on a grant title below to expand the full details for that specific grant.
20241 grants / $150,000
Investigation and development of a broad spectrum anti-viral therapy for both seasonal and pandemic influenza A viral infections$150,000
By combining new applications of unique tools, interventions, and models, and collaborations with world-leading experts in respiratory immunobiology, iron biology, and respiratory viral infection, this team has established a collaborative research program between Singapore and Australia to:
Investigate how seasonal and potentially pandemic influenza A virus (IAV) infections affect host iron metabolism and whether iron metabolism can be therapeutically targeted for the treatment of both seasonal and potentially pandemic IAV infection and infection-induced disease.
We have collected world-first pilot data to show that influenza A virus (IAV) infection alters iron metabolism in the airways and systemically, and that iron levels and iron-related metabolic processes play a crucial role in host defence, and in determining IAV-induced disease outcomes.
Funding body: APSR (Asian Pacific Society of Respirology)
Funding body | APSR (Asian Pacific Society of Respirology) |
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Project Team | Dr Alan Hsu, Dr Jemma Mayall, Prof Jay Horvat, Dr Kai Sen Tan, Prof Peter Wark |
Scheme | APSR Multi-Society Research Project |
Role | Investigator |
Funding Start | 2024 |
Funding Finish | 2025 |
GNo | |
Type Of Funding | International - Competitive |
Category | 3IFA |
UON | N |
20223 grants / $1,069,827
Implementation of lung function analyses that may facilitate earlier detection of harmful dust exposure and occupational lung disease$513,691
Funding body: Coal Services Health and Safety Trust
Funding body | Coal Services Health and Safety Trust |
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Project Team | Professor Jay Horvat, Doctor Dusan Ilic, Doctor Jemma Mayall, Professor Carole James, Conjoint Professor Peter Wark, Associate Professor Alexander Donald, Associate Professor Deborah Yates, A/Prof Brian Oliver, Dr Katrina Tonga, Dr David Meredith |
Scheme | Research Project |
Role | Investigator |
Funding Start | 2022 |
Funding Finish | 2025 |
GNo | G2100436 |
Type Of Funding | C3200 – Aust Not-for Profit |
Category | 3200 |
UON | Y |
Inhibiting ASC with small molecules for treatment of inflammatory diseases$450,136
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
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Project Team | Doctor Jemma Mayall, Professor Avril Robertson, Dr Rebecca Coll |
Scheme | Ideas Grants |
Role | Lead |
Funding Start | 2022 |
Funding Finish | 2024 |
GNo | G2200215 |
Type Of Funding | C1100 - Aust Competitive - NHMRC |
Category | 1100 |
UON | Y |
Development of an accurate biological test for the monitoring and assessment of occupational dust inhalation in high dust industries$106,000
Funding body: The University of Newcastle Research Associates Ltd (TUNRA)
Funding body | The University of Newcastle Research Associates Ltd (TUNRA) |
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Project Team | Professor Jay Horvat, Professor Andrew Fleming, Doctor Dusan Ilic, Mr Prabhasha Jayasundara, Doctor Jemma Mayall |
Scheme | Scholarships |
Role | Investigator |
Funding Start | 2022 |
Funding Finish | 2025 |
GNo | G2101352 |
Type Of Funding | Scheme excluded from IGS |
Category | EXCL |
UON | Y |
20211 grants / $5,000
Iron-ing out airway inflammation: A new treatment approach for respiratory viral infection-induced disease$5,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
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Project Team | Doctor Jemma Mayall |
Scheme | Research Grant |
Role | Lead |
Funding Start | 2021 |
Funding Finish | 2021 |
GNo | G2101065 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
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 |
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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 |
20193 grants / $105,354
Independent study on silicosis technologies$49,577
Funding body: Humanomics Pty Ltd
Funding body | Humanomics Pty Ltd |
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Project Team | Professor Carole James, Professor Jay Horvat, Doctor Jemma Mayall, Mr John Tessier |
Scheme | Entrepreneurs' Programme: Innovation Connections |
Role | Investigator |
Funding Start | 2019 |
Funding Finish | 2021 |
GNo | G1901552 |
Type Of Funding | C3100 – Aust For Profit |
Category | 3100 |
UON | Y |
Independent study on silicosis technologies$49,577
Funding body: Department of Industry, Innovation and Science
Funding body | Department of Industry, Innovation and Science |
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Project Team | Professor Carole James, Mr John Tessier, Professor Jay Horvat, Doctor Jemma Mayall |
Scheme | Entrepreneurs' Programme: Innovation Connections |
Role | Investigator |
Funding Start | 2019 |
Funding Finish | 2021 |
GNo | G1901613 |
Type Of Funding | C1700 - Aust Competitive - Other |
Category | 1700 |
UON | Y |
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 |
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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 |
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Project Team | Doctor Malcolm Starkey, Associate Professor 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 | C2400 – Aust StateTerritoryLocal – Other |
Category | 2400 |
UON | Y |
Research Supervision
Number of supervisions
Current Supervision
Commenced | Level of Study | Research Title | Program | Supervisor Type |
---|---|---|---|---|
2023 | PhD | Development of novel CAR T Therapies for Children Diagnosed with Central Nervous System Cancers | PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2022 | PhD | Developing Therapeutic Options for Chronic Pelvic Pain | PhD (Human Physiology), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2022 | PhD | Development of an Accurate Biological Test for the Monitoring and Assessment of Occupational Dust Inhalation in High Dust Industries | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2020 | PhD | The Role and Therapeutic Targeting of Novel Host Immune Factors in Viral Infection-induced Respiratory Disease | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
Past Supervision
Year | Level of Study | Research Title | Program | Supervisor Type |
---|---|---|---|---|
2022 | PhD | The Role of Inflammasomes during Chlamydia Infection | PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2021 | PhD | Characterization of Physiological and Neural Alterations in Chlamydial Reproductive Tract Infection | PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
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 -
Edit
News
News • 17 Nov 2022
Researchers discover why viral infections are worse for people with COPD
Researchers from the Hunter Medical Research Institute (HMRI) and the University of Newcastle have identified immune killer cells that are responsible for exacerbating viral infections in people with Chronic Obstructive Pulmonary Disease (COPD).
Dr Jemma Mayall
Position
Lecturer
Horvat
School of Biomedical Sciences and Pharmacy
College of Health, Medicine and Wellbeing
Contact Details
jemma.mayall@newcastle.edu.au | |
Phone | (02) 4042 0221 |
Office
Room | HMRI Building Lvl 2E Rm 2413 W2-122 |
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Building | HMRI Building |
Location | John Hunter Hospital Campus , |