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
320211 Infectious diseases 20
320404 Cellular immunology 30
320407 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
Edit

Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Journal article (12 outputs)

Year Citation Altmetrics Link
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)
DOI 10.1038/s41385-021-00414-6
Co-authors Paul Foster, Kelly Asquith, Steven Maltby, Jay Horvat, Philip Hansbro, Gerard Kaiko, Simon Keely, Hock Tay
2021 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.', J Allergy Clin Immunol, (2021)
DOI 10.1016/j.jaci.2021.10.003
Co-authors Hayley Scott, Peter Gibson, Lisa Wood, Jay Horvat, Malcolm Starkey, Philip Hansbro, Chantal Donovan, Alexandra Brown, Bronwyn Berthon
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.

DOI 10.1152/AJPENDO.00513.2019
Citations Scopus - 2Web of Science - 3
Co-authors Phillip Jobling, Dirk Vanhelden, Jay Horvat, Philip Hansbro
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]
DOI 10.1002/path.5401
Citations Scopus - 23Web of Science - 21
Co-authors Chantal Donovan, Jay Horvat, Alexandra Brown, Philip Hansbro, Liz Milward
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]
DOI 10.1183/13993003.01340-2019
Citations Scopus - 7Web of Science - 7
Co-authors Alexandra Brown, Jay Horvat, Chantal Donovan, Prabuddha Pathinayake, Paul Foster, Hock Tay, Malcolm Starkey, Peter Wark, Liz Holliday, Philip Hansbro, Liz Milward
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 - 12Web of Science - 12
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]

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.

DOI 10.1111/imr.12543
Citations Scopus - 76Web of Science - 70
Co-authors Jodie Simpson, Paul Foster, Malcolm Starkey, Philip Hansbro, Lisa Wood, Jay Horvat, Darryl Knight, Chantal Donovan
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.

DOI 10.1016/j.jaci.2016.04.038
Citations Scopus - 113Web of Science - 117
Co-authors Jay Horvat, Malcolm Starkey, Philip Hansbro, Simon Keely, Paul Foster, Joerg Mattes, Tattjhong Haw
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 - 32Web of Science - 29
Co-authors Philip Hansbro, Malcolm Starkey, Liz Milward, Jay Horvat
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.

DOI 10.1164/rccm.201609-1830OC
Citations Scopus - 158Web of Science - 156
Co-authors Katherine Baines, Jodie Simpson, Darryl Knight, Jay Horvat, Malcolm Starkey, Peter Wark, Lisa Wood, Philip Hansbro, Alexandra Brown, Peter Gibson
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 - 86Web of Science - 85
Co-authors Philip Hansbro, Malcolm Starkey, Paul Foster, Jodie Simpson, Peter Gibson, Jay Horvat, Emma Beckett
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 - 135Web of Science - 134
Co-authors John Schjenken, Philip Hansbro, Jay Horvat
Show 9 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 Jay Horvat, Peter Wark, Alan Hsu, Bridie Goggins, Philip Hansbro, Malcolm Starkey
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', JOURNAL OF IMMUNOLOGY, Washington, DC (2017)
Co-authors Jay Horvat, Philip Hansbro, Liz Milward, Chantal Donovan
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 Paul Foster, Joerg Mattes, Tattjhong Haw, Jay Horvat, Simon Keely, Philip Hansbro, Malcolm Starkey
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 Malcolm Starkey, Philip Hansbro, 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, Jay Horvat, Emma Beckett
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 Paul Foster, Jodie Simpson, Jay Horvat, Malcolm Starkey, Philip Hansbro, Emma Beckett, Peter Gibson
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 Philip Hansbro, Malcolm Starkey, Jay Horvat, Emma Beckett, Paul Foster
Show 4 more conferences
Edit

Grants and Funding

Summary

Number of grants 6
Total funding $124,904

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


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
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
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
Project Team Professor Carole James, Associate 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
Project Team Professor Carole James, Mr John Tessier, Associate 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
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 C2400 – Aust StateTerritoryLocal – Other
Category 2400
UON Y
Edit

Research Supervision

Number of supervisions

Completed1
Current2

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), College of Health, Medicine and Wellbeing, 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), College of Health, Medicine and Wellbeing, The University of Newcastle Principal Supervisor

Past Supervision

Year Level of Study Research Title Program Supervisor Type
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
Edit

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

Dr Jemma Mayall

Position

Post Doctoral Researcher
Horvat
School of Biomedical Sciences and Pharmacy
College of Health, Medicine and Wellbeing

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

,
Edit