Dr Bridie Goggins

Postdoctoral Researcher

School of Biomedical Sciences and Pharmacy

Career Summary

Biography

Dr Bridie Goggins is a postdoctoral researcher working in the Gastrointestinal Research group in the Priority Research Centre for Digestive Health and Neurogastroenterology. Her research examines inflammatory hypoxia in the gastrointestinal mucosa and the adaptive mechanisms allowing tissue and cell survival in these low oxygen environments. In particular, this work focuses on potential therapeutic targets to promote mucosal healing in the treatment of Inflammatory Bowel Diseases (IBD).

Dr Goggins was recently awarded her PhD in Immunology and Microbiology from the University of Newcastle in 2019.
During her PhD, Dr Goggins' work focused on the intrinsic adaptive mechanisms associated with inflammatory tissue hypoxia, namely the oxygen sensing molecule Hypoxia Inducible Factor (HIF)-1, and how this molecule can be pharmacologically stabilised to promote mucosal healing through its downstream signalling pathways. She examined the transcriptional, translational and functional contribution of HIF-1 mediated cell adhesion proteins, integrins, and their role in inflammatory mucosal healing. Her work aims to characterise HIF-1 mediated mucosal healing processes and how these mechanisms may be up-regulated as potential new therapeutics in the treatment of mucosal inflammatory diseases. 

Currently, Dr Goggins is continuing her research on HIF-1-mediated mechanisms of wound healing and is also involved in a number of industry projects examining potential new IBD therapies. She is also involved in establishing new veterinary surgical models for translational gastrointestinal research, and specialises in veterinary endoscopic techniques.

Qualifications

  • Doctor of Philosophy in Immunology and Microbiology, University of Newcastle
  • Bachelor of Biomedical Science (Honours), University of Newcastle

Keywords

  • Crohn's Disease
  • Epithelial cell biology
  • HIF Biology
  • Hypoxia
  • Inflammatory Bowel Disease
  • Integrins
  • Mucosal healing
  • Mucosal inflammation
  • Ulcerative Colitis

Fields of Research

Code Description Percentage
060599 Microbiology not elsewhere classified 30
060199 Biochemistry and Cell Biology not elsewhere classified 30
110307 Gastroenterology and Hepatology 40

Professional Experience

UON Appointment

Title Organisation / Department
Postdoctoral Researcher University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia
Casual Lecturer University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia

Awards

Award

Year Award
2017 Travel Award - Priority Research Centre for Digestive Health and Neurogastroenterology Travel Grant
The Priority Research Centre for Digestive Health & Neurogastroenterology, The University of Newcastle
2015 GESA Scientific Organising Committee Travel Award
Gastroenterological Society of Australia (GESA)
2015 Young Investigator Award - GESA Hepatology and Gastroenterology Research Workshop
Gastroenterological Society of Australia (GESA)

Prize

Year Award
2017 Best Student Oral Presentation - Australian Society for Medical Research Hunter Region Satellite Scientific Meeting
Australian Society for Medical Research (ASMR)
2015 Best Overall Poster Presentation – Australian Society for Medical Research Hunter Region Satellite Scientific Meeting
Australian Society for Medical Research (ASMR)

Scholarship

Year Award
2016 Jennie Thomas Post-Graduate Medical Research Scholarship
Jennie Thomas - Philanthropic Donor
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Publications

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


Journal article (8 outputs)

Year Citation Altmetrics Link
2019 Kaiko GE, Chen F, Lai C-W, Chiang I-L, Perrigoue J, Stojmirovic A, et al., 'PAI-1 augments mucosal damage in colitis.', Sci Transl Med, 11 (2019)
DOI 10.1126/scitranslmed.aat0852
Citations Scopus - 2
Co-authors Simon Keely, Gerard Kaiko, Paul Foster
2019 Liu G, Mateer SW, Hsu A, Goggins BJ, Tay H, Mathe A, et al., 'Platelet activating factor receptor regulates colitis-induced pulmonary inflammation through the NLRP3 inflammasome', Mucosal Immunology, 12 862-873 (2019)

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

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

DOI 10.1038/s41385-019-0163-3
Citations Scopus - 2Web of Science - 2
Co-authors Hock Tay, Alan Hsu, Andrea Johns, Peter Wark, Philip Hansbro, Michael Fricker, Steven Maltby, Paul Foster, Simon Keely
2018 Mateer SW, Mathe A, Bruce J, Liu G, Maltby S, Fricker M, et al., 'IL-6 Drives Neutrophil-Mediated Pulmonary Inflammation Associated with Bacteremia in Murine Models of Colitis', American Journal of Pathology, 188 1625-1639 (2018) [C1]

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

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

DOI 10.1016/j.ajpath.2018.03.016
Citations Scopus - 3Web of Science - 3
Co-authors Marjorie Walker, Jay Horvat, Robert Callister, Philip Hansbro, Simon Keely, Andrea Johns, Hock Tay, Michael Fricker, Paul Foster, Steven Maltby
2018 Fricker M, Goggins BJ, Mateer S, Jones B, Kim RY, Gellatly SL, et al., 'Chronic cigarette smoke exposure induces systemic hypoxia that drives intestinal dysfunction.', JCI insight, 3 1-19 (2018) [C1]
DOI 10.1172/jci.insight.94040
Citations Scopus - 9Web of Science - 10
Co-authors Nicholas Talley, Simon Keely, Marjorie Walker, Philip Hansbro, Michael Fricker
2018 Mroz MS, Lajczak NK, Goggins BJ, Keely S, Keely SJ, 'The bile acids, deoxycholic acid and ursodeoxycholic acid, regulate colonic epithelial wound healing', American Journal of Physiology - Gastrointestinal and Liver Physiology, 314 G378-G387 (2018) [C1]

© 2018 the American Physiological Society. The intestinal epithelium constitutes an innate barrier which, upon injury, undergoes self-repair processes known as restitution. Althou... [more]

© 2018 the American Physiological Society. The intestinal epithelium constitutes an innate barrier which, upon injury, undergoes self-repair processes known as restitution. Although bile acids are known as important regulators of epithelial function in health and disease, their effects on wound healing processes are not yet clear. Here we set out to investigate the effects of the colonic bile acids, deoxycholic acid (DCA) and ursodeoxycholic acid (UDCA), on epithelial restitution. Wound healing in T84 cell monolayers grown on transparent, permeable supports was assessed over 48 h with or without bile acids. Cell migration was measured in Boyden chambers. mRNA and protein expression were measured by RT-PCR and Western blotting. DCA (50¿150 µM) significantly inhibited wound closure in cultured epithelial monolayers and attenuated cell migration in Boyden chamber assays. DCA also induced nuclear accumulation of the farnesoid X receptor (FXR), whereas an FXR agonist, GW4064 (10 µM), inhibited wound closure. Both DCA and GW4064 attenuated the expression of CFTR Cl- channels, whereas inhibition of CFTR activity with either CFTR-inh -172 (10 µM) or GlyH-101 (25 µM) also prevented wound healing. Promoter/reporter assays revealed that FXR-induced downregulation of CFTR is mediated at the transcriptional level. In contrast, UDCA (50¿150 µM) enhanced wound healing in vitro and prevented the effects of DCA. Finally, DCA inhibited and UDCA promoted mucosal healing in an in vivo mouse model. In conclusion, these studies suggest bile acids are important regulators of epithelial wound healing and are therefore good targets for development of new drugs to modulate intestinal barrier function in disease treatment. NEW & NOTEWORTHY The secondary bile acid, deoxycholic acid, inhibits colonic epithelial wound healing, an effect which appears to be mediated by activation of the nuclear bile acid receptor, FXR, with subsequent downregulation of CFTR expression and activity. In contrast, ursodeoxycholic acid promotes wound healing, suggesting it may provide an alternative approach to prevent the losses of barrier function that are associated with mucosal inflammation in IBD patients.

DOI 10.1152/ajpgi.00435.2016
Citations Scopus - 6Web of Science - 4
Co-authors Simon Keely
2017 Marks E, Naudin C, Nolan G, Goggins BJ, Burns G, Mateer SW, et al., 'Regulation of IL-12p40 by HIF controls Th1/Th17 responses to prevent mucosal inflammation', MUCOSAL IMMUNOLOGY, 10 1224-1236 (2017) [C1]
DOI 10.1038/mi.2016.135
Citations Scopus - 7Web of Science - 7
Co-authors Nicholas Talley, Simon Keely, Martin Veysey, Robert Callister, Paul Foster, Marjorie Walker
2015 Marks E, Goggins BJ, Cardona J, Cole S, Minahan K, Mateer S, et al., 'Oral Delivery of Prolyl Hydroxylase Inhibitor: AKB-4924 Promotes Localized Mucosal Healing in a Mouse Model of Colitis.', Inflammatory bowel diseases, 21 267-275 (2015) [C1]
DOI 10.1097/mib.0000000000000277
Citations Scopus - 21Web of Science - 23
Co-authors Marjorie Walker, Simon Keely
2013 Goggins BJ, Chaney C, Radford-Smith GL, Horvat JC, Keely S, 'Hypoxia and Integrin-Mediated Epithelial Restitution during Mucosal Inflammation.', Front Immunol, 4 272 (2013) [C1]
DOI 10.3389/fimmu.2013.00272
Citations Scopus - 28Web of Science - 28
Co-authors Simon Keely, Jay Horvat
Show 5 more journal articles

Conference (9 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 Peter Wark, Alan Hsu, Malcolm Starkey, Philip Hansbro, Jay Horvat
2017 Goggins BJ, Minahan K, Outteridge N, Knight D, Horvat J, Keely S, 'Hypoxia Inducible Factor (HIF)-1 accelerates epithelial wound healing through integrin regulation', FASEB JOURNAL, Chicago, IL (2017)
Co-authors Darryl Knight, Simon Keely, Jay Horvat
2017 Lajczak NK, Ward JB, Goggins BJ, Keely S, Keely SJ, 'Bacterial metabolism of Ursodeoxycholic Acid is necessary for its protective actions in a mouse model of intestinal inflammation', FASEB JOURNAL, Chicago, IL (2017)
Co-authors Simon Keely
2017 Marks E, Naudin C, Walker MM, Veysey M, Foster P, Talley NJ, et al., 'REGULATION OF IL-12P40 BY HIF CONTROLS TH1/TH17 RESPONSES TO PREVENT MUCOSAL INFLAMMATION', GASTROENTEROLOGY, Chicago, IL (2017)
DOI 10.1016/S0016-5085(17)32053-X
Citations Web of Science - 1
Co-authors Paul Foster, Robert Callister, Marjorie Walker, Nicholas Talley, Martin Veysey, Simon Keely
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, Philip Hansbro, Simon Keely, Steven Maltby
2014 Goggins B, Minahan K, Marks E, Mateer S, Cardona J, Knight D, et al., 'Hypoxia inducible factor (HIF)-1 accelerates epithelial wound healing through integrin regulation', JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY (2014) [E3]
Co-authors Simon Keely, Jay Horvat, Darryl Knight
2014 Cardona J, Marks E, Goggins B, Mateer S, Minahan K, Horvat J, Keely S, 'The role of antibiotics in the development of food allergy', JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY (2014) [E3]
Co-authors Simon Keely, Jay Horvat
2014 Marks E, Nolan G, Mateer S, Minahan K, Goggins B, Cardona J, Keely S, 'Hypoxia inducible factor 1 alpha (HIF-1 alpha) regulates anti-inflammatory lymphoid responses during colitis', JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY (2014) [E3]
Co-authors Simon Keely
2014 Mateer S, Maltby S, Marks E, Goggins B, Horvat J, Hansbro P, Keely S, 'Immune cell mis-homing drives secondary organ inflammation in inflammatory bowel disease; a focus on the respiratory system', JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY (2014) [E3]
Co-authors Jay Horvat, Steven Maltby, Philip Hansbro, Simon Keely
Show 6 more conferences
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Grants and Funding

Summary

Number of grants 1
Total funding $129,866

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


20191 grants / $129,866

In vivo and in vitro study of HIF stabilization through prolyla hydroxylase inhibition$129,866

Funding body: Gossamer Bio Inc

Funding body Gossamer Bio Inc
Project Team Associate Professor Simon Keely, Doctor Bridie Goggins
Scheme Research Grant
Role Investigator
Funding Start 2019
Funding Finish 2019
GNo G1900382
Type Of Funding C3211 - International For profit
Category 3211
UON Y
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Dr Bridie Goggins

Positions

Postdoctoral Researcher
Gastrointestinal Research Group
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Casual Lecturer
Gastrointestinal Research Group
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Contact Details

Email bridie.goggins@newcastle.edu.au
Phone (02) 4042 0283

Office

Room Level 3 - East Wing
Building Hunter Medical Research Institute (HMRI)
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