Professor Simon Keely

Professor Simon Keely

Professor

School of Biomedical Sciences and Pharmacy (Immunology and Microbiology)

Career Summary

Biography

Dr. Keely graduated with a Ph.D. from University College Dublin. He undertook postdoctoral research training at the Mucosal Inflammation Program in University of Colorado Denver funded by a fellowship from the Crohn's and Colitis Foundation of America. Dr. Keely is chief investigator of the Hunter Medical Research Institute (HMRI) Gastrointestinal Research Group. The group's current research program examines molecular mechanisms of disease in the gastrointestinal tract.

The Gastrointestinal Research Group is focused on studying the cellular processes of digestive disease and infection. The group is particularly interested in mucosal inflammation and how tissues adapt to conditions of oxygen deficiency (hypoxia) in inflamed tissue. This is particularly relevant to chronic inflammatory diseases such as the inflammatory bowel diseases (IBD); Crohn's disease & ulcerative colitis. To achieve this, we study cellular mechanisms of inflammation and adaption to inflammation in vitro. We give our findings physiological context by applying them to in vivo models of IBD and then, through our collaborators at John Hunter Hospital, examine human context in patient samples. With this approach, we hope to identify strategies for new therapeutic approaches to treating IBD.

Our current, ongoing research includes:

1) Investigating how wound healing is regulated in the intestine during the inflammation associated with Crohn's disease.

2) Examining the mechanisms leading to IBD-related disease that occurs outside of the gastrointestinal tract.

3) Understanding the immunology of functional gastrointestinal disorders.

4) Examining how inflammation and host-microbe interactions influence surgical outcomes. 



Qualifications

  • PhD, University College, Dublin - Ireland

Keywords

  • Cell Biology
  • Crohn's Disease
  • Epithelial Biology
  • HIF Biology
  • Hypoxia
  • Immunology
  • Infection
  • Inflammatory Bowel Disease
  • Microbiology
  • Molecular Biology
  • Mucosal Inflammation
  • Ulcerative Colitis
  • clinical science
  • host-pathogen interactions
  • microbiome

Languages

  • Irish (Fluent)

Professional Experience

UON Appointment

Title Organisation / Department
Professor University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia
Professor University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia

Academic appointment

Dates Title Organisation / Department
1/12/2009 - 1/2/2011 Senior Instructor

Crohn's & Colitis Foundation of America Research Fellow

University of Colorado, Denver
United States
1/12/2008 - 1/12/2009 Instructor University of Colorado, Denver
United States
1/11/2008 - 1/1/2010 Instructor

Junior Faculty

University of Colorado, Denver
Mucosal Inflammation Program
United States
1/10/2005 - 1/7/2006 Postdoctoral Research Fellow University College Dublin
School of Veterinary Medicine
Ireland
1/1/2012 -  Membership - NHMRC GRP NHMRC GRP
Australia
1/1/2011 -  Membership - Australian Society for Immunology Australian Society for Immunology
Australia
1/1/2011 -  Membership - Gastroenterological Society of Australia Gastroenterological Society of Australia (GESA)
1/7/2006 - 1/11/2008 Postdoctoral Research Fellow University of Colorado, Denver
Mucosal Inflammation Program
United States
1/1/2010 - 1/2/2011 Senior Instructor University of Colorado, Denver
Mucosal Inflammation Program
United States
1/1/2017 -  Associate Professor Faculty of Health, University of Newcastle
Australia

Professional appointment

Dates Title Organisation / Department
8/10/2015 -  Gastrointestinal Research Group Leader Hunter Medical Research Institute (HMRI)
Viruses, Infection/Immunity, Vaccines and Asthma Program
Australia
1/1/2014 -  Scientific Advisory Board Aetheria Therapeutics
United States
1/1/2013 - 1/12/2014 Scientific Consultant Janssen Cilag Pty Ltd

Awards

Prize

Year Award
2014 John Forte GI/Liver Plenary Award for Distinguished Abstract
American Physiological Society
2011 Outstanding Paper Award - GI Response to Injury
American Gastroenterological Association
2009 Outstanding Paper Award, Advances in IBD
Crohn's and Colitis Foundation of America

Research Award

Year Award
2009 Research Fellowship
Crohn's and Colitis Foundation of America

Thesis Examinations

Year Level Discipline Thesis
2015 PHD Health Immunology and IBD
2015 PHD Health Immunology and IBD
2015 PHD Health Immunology and IBD

Grant Reviews

Year Grant Amount
2013 Project Grant GRP
Aust Competitive - Commonwealth - 1CS, Aust Competitive - Commonwealth - 1CS
$0
2012 Project Grant GRP
Aust Competitive - Commonwealth - 1CS, Aust Competitive - Commonwealth - 1CS
$0
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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
2019 Bruce J, Kaiko GE, Keely S, 'Isolation and in vitro culture of human gut progenitor cells', Methods in Molecular Biology, Humana, New York, NY 49-62 (2019) [B1]
DOI 10.1007/978-1-4939-9631-5_5
Co-authors Gerard Kaiko
2018 Hollins SL, Bruce J, Keely S, Hodgson D, 'The Gut-Brain Axis in Neuropsychopathology', Advances in Psychobiology, Nova Science Publishers, Hauppauge, NY 11788-3619 USA 189-218 (2018) [B1]
Citations Scopus - 1
Co-authors Deborah Hodgson

Journal article (85 outputs)

Year Citation Altmetrics Link
2021 Turner A, Veysey M, Keely S, Scarlett CJ, Lucock M, Beckett EL, 'Genetic Variation in the Bitter Receptors Responsible for Epicatechin Detection Are Associated with BMI in an Elderly Cohort', NUTRIENTS, 13 (2021) [C1]
DOI 10.3390/nu13020571
Co-authors Emma Beckett, Mark Lucock, C Scarlett, Martin Veysey
2021 Duncanson K, Burns G, Pryor J, Keely S, Talley NJ, 'Mechanisms of Food-Induced Symptom Induction and Dietary Management in Functional Dyspepsia.', Nutrients, 13 (2021)
DOI 10.3390/nu13041109
Co-authors Kerith Duncanson, Nicholas Talley
2021 Goggins BJ, Minahan K, Sherwin S, Soh WS, Pryor J, Bruce J, et al., 'Pharmacological HIF-1 stabilization promotes intestinal epithelial healing through regulation of a-integrin expression and function.', Am J Physiol Gastrointest Liver Physiol, 320 G420-G438 (2021)
DOI 10.1152/ajpgi.00192.2020
Co-authors Darryl Knight, Bridie Goggins, Marjorie Walker, Andrea Johns, Jay Horvat
2021 Alemao CA, Budden KF, Gomez HM, Rehman SF, Marshall JE, Shukla SD, et al., 'Impact of diet and the bacterial microbiome on the mucous barrier and immune disorders.', Allergy, 76 714-734 (2021)
DOI 10.1111/all.14548
Citations Scopus - 2Web of Science - 2
Co-authors Philip Hansbro, Chantal Donovan
2020 Liu G, Baird AW, Parsons MJ, Fan K, Skerrett-Byrne DA, Nair PM, et al., 'Platelet activating factor receptor acts to limit colitis-induced liver inflammation', FASEB JOURNAL, 34 7718-7732 (2020) [C1]
DOI 10.1096/fj.201901779R
Citations Scopus - 2Web of Science - 1
Co-authors Bridie Goggins, Andrea Johns, David Skerrett-Byrne, Hock Tay, Brett Nixon, Philip Hansbro
2020 Shah A, Talley NJ, Koloski N, Macdonald GA, Kendall BJ, Shanahan ER, et al., 'Duodenal bacterial load as determined by quantitative polymerase chain reaction in asymptomatic controls, functional gastrointestinal disorders and inflammatory bowel disease', Alimentary Pharmacology and Therapeutics, 52 155-167 (2020) [C1]

Background: Small intestinal bacterial overgrowth may play a role in gastrointestinal and non-gastrointestinal diseases. Aims: To use quantitative polymerase chain reaction (qPCR)... [more]

Background: Small intestinal bacterial overgrowth may play a role in gastrointestinal and non-gastrointestinal diseases. Aims: To use quantitative polymerase chain reaction (qPCR) to determine and compare bacterial loads of duodenal biopsies in asymptomatic controls, and patients with functional gastrointestinal disorders (FGIDs) and inflammatory bowel disease (IBD) including ulcerative colitis (UC) and Crohn¿s disease (CD). To define effects of gastric acid inhibition on bacterial load, explore links of bacterial load and gastrointestinal symptoms in response to a standardised nutrient challenge and compare bacterial load with glucose breath test results. Methods: In 237 patients (63 controls, 84 FGID and 90 IBD), we collected mucosal samples under aseptic conditions during endoscopy extracted and total DNA. Bacterial load metric was calculated utilising qPCR measurements of the bacterial 16S rRNA gene, normalised to human beta-actin expression. Standard glucose breath test and nutrient challenge test were performed. Results: The duodenal microbial load was higher in patients with FGID (0.22¿±¿0.03) than controls (0.07¿±¿0.05; P¿=¿0.007) and patients with UC (0.01¿±¿0.05) or CD (0.02¿±¿0.09), (P¿=¿0.0001). While patients treated with proton pump inhibitors (PPI) had significantly higher bacterial loads than non-users (P¿<¿0.05), this did not explain differences between patient groups and controls. Bacterial load was significantly (r¿=¿0.21, P¿<¿0.016) associated with the symptom response to standardised nutrient challenge test. Methane, but not hydrogen values on glucose breath test were associated with bacterial load measured utilising qPCR. Conclusions: Utilising qPCR, a diagnosis of FGID and treatment with PPI were independently associated with increased bacterial loads. Increased bacterial loads are associated with an augmented symptom response to a standardised nutrient challenge.

DOI 10.1111/apt.15786
Citations Scopus - 2Web of Science - 3
Co-authors Nicholas Talley, Marjorie Walker
2020 Prasad SS, Keely S, Talley NJ, Kairuz T, Walker MM, 'Pharmacists' Confidence in Managing Patients with Inflammatory Bowel Disease.', Pharmacy, 8 (2020) [C1]
DOI 10.3390/pharmacy8020068
Co-authors Marjorie Walker, Nicholas Talley, Therese Kairuz
2020 Prasad SS, Potter M, Keely S, Talley NJ, Walker MM, Kairuz T, 'Roles of healthcare professionals in the management of chronic gastrointestinal diseases with a focus on primary care: A systematic review', JGH Open, 4 221-229 (2020) [C1]
DOI 10.1002/jgh3.12235
Citations Scopus - 1
Co-authors Marjorie Walker, Therese Kairuz, Nicholas Talley
2020 Sokulsky LA, Goggins B, Sherwin S, Eyers F, Kaiko GE, Board PG, et al., 'GSTO1-1 is an upstream suppressor of M2 macrophage skewing and HIF-1 alpha-induced eosinophilic airway inflammation', CLINICAL AND EXPERIMENTAL ALLERGY, 50 609-624 (2020) [C1]
DOI 10.1111/cea.13582
Citations Scopus - 3Web of Science - 2
Co-authors Ming Yang, Paul Foster, Gerard Kaiko, Bridie Goggins
2020 Potter MDE, Jones MP, Walker MM, Koloski NA, Keely S, Holtmann G, Talley AC NJ, 'Incidence and prevalence of self-reported non-coeliac wheat sensitivity and gluten avoidance in Australia', Medical Journal of Australia, 212 126-131 (2020) [C1]
DOI 10.5694/mja2.50458
Citations Scopus - 5Web of Science - 3
Co-authors Nicholas Talley, Marjorie Walker
2020 Makanyengo SO, Carroll GM, Goggins BJ, Smith SR, Pockney PG, Keely S, 'Systematic Review on the Influence of Tissue Oxygenation on Gut Microbiota and Anastomotic Healing', JOURNAL OF SURGICAL RESEARCH, 249 186-196 (2020) [C1]
DOI 10.1016/j.jss.2019.12.022
Citations Scopus - 1Web of Science - 1
Co-authors Peter Pockney, Bridie Goggins, Stephen Smith
2020 deZoeten EF, Battista KD, Colson SB, Lovell MA, Kessler BE, Isfort RW, et al., 'Markers of Hypoxia Correlate with Histologic and Endoscopic Severity of Colitis in Inflammatory Bowel Disease.', Hypoxia (Auckland, N.Z.), 8 1-12 (2020) [C1]
DOI 10.2147/hp.s219049
2020 Talley NJ, Irani M, Keely S, 'Bacterial therapy for irritable bowel syndrome', LANCET GASTROENTEROLOGY & HEPATOLOGY, 5 627-629 (2020)
DOI 10.1016/S2468-1253(20)30079-0
Citations Web of Science - 1
Co-authors Nicholas Talley
2020 Turner A, Veysey M, Keely S, Scarlett CJ, Lucock M, Beckett EL, 'Intense sweeteners, taste receptors and the gut microbiome: A metabolic health perspective', International Journal of Environmental Research and Public Health, 17 1-18 (2020) [C1]
DOI 10.3390/ijerph17114094
Co-authors Emma Beckett, Martin Veysey, Mark Lucock, C Scarlett
2020 Carroll GM, Burns GL, Petit JA, Walker MM, Mathe A, Smith SR, et al., 'Does postoperative inflammation or sepsis generate neutrophil extracellular traps that influence colorectal cancer progression? A systematic review', Surgery Open Science, 2 57-69 (2020) [C1]
DOI 10.1016/j.sopen.2019.12.005
Co-authors Peter Pockney, Andrea Johns, Stephen Smith, Marjorie Walker
2020 Talley NJ, Holtmann GJ, Jones M, Koloski NA, Walker MM, Burns G, et al., 'Zonulin in serum as a biomarker fails to identify the IBS, functional dyspepsia and non-coeliac wheat sensitivity', GUT, 69 1719-1722 (2020)
DOI 10.1136/gutjnl-2019-318664
Citations Scopus - 6Web of Science - 4
Co-authors Marjorie Walker, Nicholas Talley
2020 Potter MDE, Duncanson K, Jones MP, Walker MM, Keely S, Talley NJ, 'Wheat sensitivity and functional dyspepsia: A pilot, double-blind, randomized, placebo-controlled dietary crossover trial with novel challenge protocol', Nutrients, 12 1-15 (2020) [C1]

Introduction: Functional dyspepsia (FD), characterised by symptoms of epigastric pain or early satiety and post prandial distress, has been associated with duodenal eosinophilia, ... [more]

Introduction: Functional dyspepsia (FD), characterised by symptoms of epigastric pain or early satiety and post prandial distress, has been associated with duodenal eosinophilia, raising the possibility that it is driven by an environmental allergen. Non-coeliac gluten or wheat sensitivity (NCG/WS) has also been associated with both dyspeptic symptoms and duodenal eosinophilia, suggesting an overlap between these two conditions. The aim of this study was to evaluate the role of wheat (specifically gluten and fructans) in symptom reduction in participants with FD in a pilot randomized double-blind, placebo controlled, dietary crossover trial. Methods: Patients with Rome III criteria FD were recruited from a single tertiary centre in Newcastle, Australia. All were individually counselled on a diet low in both gluten and fermentable oligo-, di-, mono-saccharides, and polyols (FODMAPs) by a clinical dietitian, which was followed for four weeks (elimination diet phase). Those who had a >30% response to the run-in diet, as measured by the Nepean Dyspepsia Index, were then re-challenged with ¿muesli¿ bars containing either gluten, fructan, or placebo in randomised order. Those with symptoms which significantly reduced during the elimination diet, but reliably reappeared (a mean change in overall dyspeptic symptoms of >30%) with gluten or fructan re-challenge were deemed to have wheat induced FD. Results: Eleven participants were enrolled in the study (75% female, mean age 43 years). Of the initial cohort, nine participants completed the elimination diet phase of whom four qualified for the rechallenge phase. The gluten-free, low FODMAP diet led to an overall (albeit non-significant) improvement in symptoms of functional dyspepsia in the diet elimination phase (mean NDI symptom score 71.2 vs. 47.1, p = 0.087). A specific food trigger could not be reliably demonstrated. Conclusions: Although a gluten-free, low-FODMAP diet led to a modest overall reduction in symptoms in this cohort of FD patients, a specific trigger could not be identified. The modified Salerno criteria for NCG/WS identification trialled in this dietary rechallenge protocol was fit-for-purpose. However, larger trials are required to determine whether particular components of wheat induce symptoms in functional dyspepsia.

DOI 10.3390/nu12071947
Citations Scopus - 3Web of Science - 1
Co-authors Marjorie Walker, Kerith Duncanson, Nicholas Talley
2020 Prasad SS, Duncanson K, Keely S, Talley NJ, Kairuz T, Holtmann GJ, et al., 'A Role for Primary Care Pharmacists in the Management of Inflammatory Bowel Disease? Lessons from Chronic Disease: A Systematic Review.', Pharmacy (Basel), 8 1-13 (2020) [C1]
DOI 10.3390/pharmacy8040204
Co-authors Therese Kairuz, Marjorie Walker, Kerith Duncanson, Nicholas Talley
2020 Wauters L, Burns G, Ceulemans M, Walker MM, Vanuytsel T, Keely S, Talley NJ, 'Duodenal inflammation: an emerging target for functional dyspepsia?', Expert Opinion on Therapeutic Targets, 24 511-523 (2020) [C1]

Introduction: Functional dyspepsia (FD) is one of the most common functional gastrointestinal disorders and is classified into postprandial distress and epigastric pain syndrome. ... [more]

Introduction: Functional dyspepsia (FD) is one of the most common functional gastrointestinal disorders and is classified into postprandial distress and epigastric pain syndrome. Despite the recognition of duodenal inflammation as a potential trigger of symptoms, only limited anti-inflammatory therapies exist. Areas covered: This narrative review summarizes the recent advances in the pathophysiology and treatment of FD; it identifies potential therapeutic targets and gaps in the field. An electronic literature search was conducted in Pubmed up to 31st of December 2019. Expert opinion: There is compelling evidence for the role of duodenal inflammation and the eosinophil-mast cell axis in the pathogenesis of dyspeptic symptoms. Traditional prokinetic drugs and neuromodulators target gastric dysmotility and visceral hypersensitivity but are hampered by limited efficacy and side effects. Independent of acid suppression, the anti-inflammatory action of proton pump inhibitors, which remain the first-line therapy in FD, may also explain their therapeutic effect. Other existing and newly established anti-inflammatory drugs should be investigated while trials including probiotics and selective antibiotics should examine the host microbiome and immune activation. Targeted treatments for potential causes of duodenal pathology, such as impaired permeability and dysbiosis, are likely to emerge in the future.

DOI 10.1080/14728222.2020.1752181
Citations Scopus - 3Web of Science - 2
Co-authors Nicholas Talley, Marjorie Walker
2020 Keely S, Talley NJ, 'Duodenal bile acids as determinants of intestinal mucosal homeostasis and disease', NEUROGASTROENTEROLOGY AND MOTILITY, 32 (2020) [C1]
DOI 10.1111/nmo.13854
Citations Scopus - 2
Co-authors Nicholas Talley
2020 Pryor J, Burns GL, Duncanson K, Horvat JC, Walker MM, Talley NJ, Keely S, 'Functional Dyspepsia and Food: Immune Overlap with Food Sensitivity Disorders.', Current gastroenterology reports, 22 (2020) [C1]
DOI 10.1007/s11894-020-00789-9
Citations Scopus - 1
Co-authors Kerith Duncanson, Jay Horvat, Marjorie Walker, Nicholas Talley
2019 B Biomed GB, Carroll G, Mathe A, Horvat J, Foster P, Walker MM, et al., 'Evidence for Local and Systemic Immune Activation in Functional Dyspepsia and the Irritable Bowel Syndrome: A Systematic Review', American Journal of Gastroenterology, 114 429-436 (2019) [C1]

BACKGROUND:Subtle histopathologic features such as eosinophilia and increased mast cells have been observed in functional gastrointestinal disorders (FGIDs), including functional ... [more]

BACKGROUND:Subtle histopathologic features such as eosinophilia and increased mast cells have been observed in functional gastrointestinal disorders (FGIDs), including functional dyspepsia (FD) and the irritable bowel syndrome (IBS). The mechanisms that drive recruitment of these cells to the gastrointestinal tract remain unexplained, largely due to the heterogeneity in phenotypes among patients diagnosed with such conditions. We aimed to systematically review the literature and collate the evidence for immune activation in FD and IBS, and where possible, detail the nature of activation.METHODS:Seven literature databases were searched using the keywords: 'functional gastrointestinal disorder', FGID, 'functional dyspepsia', 'non-ulcer dyspepsia', 'idiopathic dyspepsia', 'irritable bowel syndrome', IBS and 'immun*'.RESULTS:Fifty-one papers reporting discordant immune features met the selection criteria for this review. Changes in lymphocyte populations, including B and T lymphocyte numbers and activation status were reported in IBS and FD, in conjunction with duodenal eosinophilia in FD and increased colonic mast cells in IBS. Increases in circulating a4 ß7 gut-homing T cells appear to be linked to the pathophysiology of both FD and IBS. Studies in the area are complicated by poor phenotyping of patients into subgroups and the subtle nature of the immune activity involved in FD and IBS.CONCLUSIONS:Alterations in proportions of gut-homing T lymphocytes in both FD and IBS indicate that a loss of mucosal homeostasis may drive the symptoms of FD and IBS. There is indirect evidence that Th17 responses may play a role in FGIDs, however the evidence for a Th2 immune phenotype in FD and IBS is limited. Although immune involvement is evident, large, well-characterised patient cohorts are required to elucidate the immune mechanisms driving the development of FGIDs. + +

DOI 10.1038/s41395-018-0377-0
Citations Scopus - 37Web of Science - 28
Co-authors Andrea Johns, Nicholas Talley, Paul Foster, Marjorie Walker, Jay Horvat
2019 Shah A, Crawford D, Burger D, Martin N, Walker M, Talley NJ, et al., 'Effects of Antibiotic Therapy in Primary Sclerosing Cholangitis with and without Inflammatory Bowel Disease: A Systematic Review and Meta-Analysis', Seminars in Liver Disease, 39 432-441 (2019) [C1]

The authors conducted a systematic review and meta-analysis to assess the effect of antibiotic therapy in primary sclerosing cholangitis (PSC). Effect of antibiotic therapy on May... [more]

The authors conducted a systematic review and meta-analysis to assess the effect of antibiotic therapy in primary sclerosing cholangitis (PSC). Effect of antibiotic therapy on Mayo PSC Risk Score (MRS), serum alkaline phosphatase (ALP), total serum bilirubin (TSB), and adverse events (AEs) rates were calculated and expressed as standardized difference of means or proportions. Five studies including 124 PSC patients who received antibiotics were included. Overall, antibiotic treatment was associated with a statistically significant reduction in ALP, MRS, and TSB by 33.2, 36.1, and 28.8%, respectively. ALP reduction was greatest for vancomycin (65.6%, p < 0.002) and smallest with metronidazole (22.7%, p = 0.18). Overall, 8.9% (95% confidence interval: 3.9-13.9) of patients had AEs severe enough to discontinue antibiotic therapy. In PSC patients, antibiotic treatment results in a significant improvement in markers of cholestasis and MRS. Antibiotics, particularly vancomycin, may have a positive effect on PSC either via direct effects on the microbiome or via host-mediated mechanisms.

DOI 10.1055/s-0039-1688501
Citations Scopus - 10Web of Science - 10
Co-authors Marjorie Walker, Nicholas Talley
2019 Shukla SD, Walters EH, Simpson JL, Keely S, Wark PAB, O'Toole RF, Hansbro PM, 'Hypoxia-inducible factor and bacterial infections in chronic obstructive pulmonary disease', RESPIROLOGY, 25 53-63 (2019) [C1]
DOI 10.1111/resp.13722
Citations Scopus - 5Web of Science - 4
Co-authors Philip Hansbro, Peter Wark, Jodie Simpson
2019 Burns G, Pryor J, Holtmann G, Walker MM, Talley NJ, Keely S, 'Immune Activation in Functional Gastrointestinal Disorders.', Gastroenterology & hepatology, 15 539-548 (2019) [C1]
Citations Scopus - 5
Co-authors Marjorie Walker, Nicholas Talley
2019 Turner A, Chijoff E, Veysey M, Keely S, Scarlett CJ, Lucock M, Beckett EL, 'Interactions between taste receptors and the gastrointestinal microbiome in inflammatory bowel disease', Journal of Nutrition and Intermediary Metabolism, 18 (2019) [C1]
DOI 10.1016/j.jnim.2019.100106
Citations Scopus - 5
Co-authors Emma Beckett, Mark Lucock, Martin Veysey, C Scarlett, Eileen Chijoff Uon
2019 Walker MM, Talley NJ, Keely S, 'Follow up on atopy and the gastrointestinal tract - a review of a common association 2018.', Expert review of gastroenterology & hepatology, 13 437-445 (2019) [C1]
DOI 10.1080/17474124.2019.1596025
Citations Scopus - 1Web of Science - 1
Co-authors Marjorie Walker, Nicholas Talley
2019 Parsons MJ, Keely S, 'FOXO3 Loss Drives Inflammation-Associated CRC: The Consequences of Being (Knock)Out-FOX'd', CELLULAR AND MOLECULAR GASTROENTEROLOGY AND HEPATOLOGY, 7 295-296 (2019)
DOI 10.1016/j.jcmgh.2018.11.003
Citations Scopus - 1
2019 Koloski N, Jones M, Walker MM, Veysey M, Zala A, Keely S, et al., 'Population based study: atopy and autoimmune diseases are associated with functional dyspepsia and irritable bowel syndrome, independent of psychological distress', Alimentary Pharmacology and Therapeutics, 49 546-555 (2019) [C1]

Background: The pathogenesis of functional GI disorders (FGIDs) is uncertain. However, underlying immune activation and psychological distress has been documented in irritable bow... [more]

Background: The pathogenesis of functional GI disorders (FGIDs) is uncertain. However, underlying immune activation and psychological distress has been documented in irritable bowel syndrome (IBS) and functional dyspepsia (FD). Epidemiological data from the UK suggest that FGIDs are linked to atopy and certain autoimmune diseases but this has not been confirmed. Aim: To test if allergic or autoimmune diseases are independently associated with FGIDs, irrespective of psychological distress in a large population based study. Methods: A total of 3542 people (mean age 57.9¿years and 52.7% females) randomly selected from the Australian population, returned a mail survey (response rate¿=¿43%). The survey asked about a physician diagnosis of autoimmune disease (scleroderma, psoriasis, rheumatoid arthritis and diabetes mellitus) or allergic conditions (asthma, food, pollen and/or animal allergy). The questionnaire assessed psychological distress and Rome III criteria for FD and IBS. Results: Asthma, food, pollen and animal allergies, psoriasis and rheumatoid arthritis were univariately significantly associated with IBS and FD. Food allergy (OR¿=¿1.66; 95% CI¿=¿1.15-2.40, P¿=¿0.007), psoriasis (OR¿=¿1.81; 95% CI¿=¿1.19-2.74, P¿=¿0.006) and rheumatoid arthritis (OR¿=¿1.68; 95% CI¿=¿1.15-2.4, P¿=¿0.007) were independent risk factors for IBS, controlling for age, gender and psychological distress. In FD, asthma (OR¿=¿1.32; 95% CI¿=¿1.04-1.68, P¿=¿0.025) and food allergy (OR¿=¿1.78; 95% CI¿=¿1.28-2.49, P¿=¿0.001) were independent predictors, controlling for age, sex and psychological distress. Conclusions: There is evidence that both atopic and autoimmune diseases are risk factors for FGIDs, independent of psychological distress, differing in IBS and FD. This provides evidence that different peripheral pathways may be involved in the pathogenesis of certain FGIDs.

DOI 10.1111/apt.15120
Citations Scopus - 26Web of Science - 24
Co-authors Martin Veysey, Marjorie Walker, Nicholas Talley
2019 Keely S, Talley NJ, 'In the ZOne: How Impedance Facilitates Progress in Functional Dyspepsia Research', DIGESTIVE DISEASES AND SCIENCES, 64 3027-3029 (2019)
DOI 10.1007/s10620-019-05575-w
Citations Scopus - 2
Co-authors Nicholas Talley
2019 Duncanson K, Burrows T, Keely S, Potter M, Das G, Walker M, Talley NJ, 'The alignment of dietary intake and symptom-reporting capture periods in studies assessing associations between food and functional gastrointestinal disorder symptoms: A systematic review', Nutrients, 11 (2019) [C1]

Food ingestion is heavily implicated in inducing symptoms of irritable bowel syndrome (IBS) and functional dyspepsia (FD), which affect over one-third of adults in developed count... [more]

Food ingestion is heavily implicated in inducing symptoms of irritable bowel syndrome (IBS) and functional dyspepsia (FD), which affect over one-third of adults in developed countries. The primary aim of this paper was to assess the alignment of dietary assessment and symptom-reporting capture periods in diet-related studies on IBS or FD in adults. Secondary aims were to compare the degree of alignment, validity of symptom-reporting tools and reported significant associations between food ingestion and symptoms. A five-database systematic literature search resulted in 40 included studies, from which data were extracted and collated. The food/diet and symptom capture periods matched exactly in 60% (n = 24/40) of studies, overlapped in 30% (n = 12/40) of studies and were not aligned in 10% (n = 4/40) of studies. Only 30% (n = 12/40) of studies that reported a significant association between food and global gastrointestinal symptoms used a validated symptom-reporting tool. Of the thirty (75%) studies that reported at least one significant association between individual gastrointestinal symptoms and dietary intake, only four (13%) used a validated symptom tool. Guidelines to ensure that validated symptom-reporting tools are matched with fit-for-purpose dietary assessment methods are needed to minimise discrepancies in the alignment of food and symptom tools, in order to progress functional gastrointestinal disorder research.

DOI 10.3390/nu11112590
Citations Scopus - 3Web of Science - 1
Co-authors Marjorie Walker, Tracy Burrows, Kerith Duncanson, Nicholas Talley
2019 Shukla SD, Shastri MD, Chong WC, Dua K, Budden KF, Mahmood MQ, et al., 'Microbiome-focused asthma management strategies', Current Opinion in Pharmacology, 46 143-149 (2019) [C1]

Asthma is a common, heterogeneous and serious disease with high prevalence globally. Poorly controlled, steroid-resistant asthma is particularly important as there are no effectiv... [more]

Asthma is a common, heterogeneous and serious disease with high prevalence globally. Poorly controlled, steroid-resistant asthma is particularly important as there are no effective therapies and it exerts substantial healthcare and societal burden. The role of microbiomes, particularly in chronic diseases has generated considerable interest in recent times. Existing evidence clearly demonstrates an association between asthma initiation and the microbiome, both respiratory and gastro-intestinal, although its¿ roles are poorly understood when assessing the asthma progression or heterogeneity (i.e. phenotypes/endotypes) across different geographical locations. Moreover, modulating microbiomes could be preventive and/or therapeutic in patients with asthma warrants urgent attention. Here, we review recent advances in assessing the role of microbiomes in asthma and present the challenges associated with the potential therapeutic utility of modifying microbiomes in management.

DOI 10.1016/j.coph.2019.06.003
Citations Scopus - 4Web of Science - 4
Co-authors Nicole Hansbro, Philip Hansbro
2019 Budden KF, Shukla SD, Rehman SF, Bowerman KL, Keely S, Hugenholtz P, et al., 'Functional effects of the microbiota in chronic respiratory disease', The Lancet Respiratory Medicine, 7 907-920 (2019) [C1]

The composition of the lung microbiome is increasingly well characterised, with changes in microbial diversity or abundance observed in association with several chronic respirator... [more]

The composition of the lung microbiome is increasingly well characterised, with changes in microbial diversity or abundance observed in association with several chronic respiratory diseases such as asthma, cystic fibrosis, bronchiectasis, and chronic obstructive pulmonary disease. However, the precise effects of the microbiome on pulmonary health and the functional mechanisms by which it regulates host immunity are only now beginning to be elucidated. Bacteria, viruses, and fungi from both the upper and lower respiratory tract produce structural ligands and metabolites that interact with the host and alter the development and progression of chronic respiratory diseases. Here, we review recent advances in our understanding of the composition of the lung microbiome, including the virome and mycobiome, the mechanisms by which these microbes interact with host immunity, and their functional effects on the pathogenesis, exacerbations, and comorbidities of chronic respiratory diseases. We also describe the present understanding of how respiratory microbiota can influence the efficacy of common therapies for chronic respiratory disease, and the potential of manipulation of the microbiome as a therapeutic strategy. Finally, we highlight some of the limitations in the field and propose how these could be addressed in future research.

DOI 10.1016/S2213-2600(18)30510-1
Citations Scopus - 62Web of Science - 53
Co-authors Philip Hansbro
2019 Burns G, Carroll G, Mathe A, Horvat J, Foster P, Walker MM, et al., 'Evidence for Local and Systemic Immune Activation in Functional Dyspepsia and the Irritable Bowel Syndrome: A Systematic Review.', Am J Gastroenterol, 114 429-436 (2019)
DOI 10.1038/s41395-018-0377-0
2019 Talley NJ, Holtmann G, Walker MM, Burns G, Potter M, Shah A, et al., 'Circulating Anti-cytolethal Distending Toxin B and Anti-vinculin Antibodies as Biomarkers in Community and Healthcare Populations With Functional Dyspepsia and Irritable Bowel Syndrome.', Clin Transl Gastroenterol, 10 e00064 (2019) [C1]
DOI 10.14309/ctg.0000000000000064
Citations Scopus - 8Web of Science - 9
Co-authors Marjorie Walker, Nicholas Talley
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) [C1]

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 patient... [more]

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 - 18Web of Science - 15
Co-authors Hock Tay, Paul Foster, Michael Fricker, Bridie Goggins, Peter Wark, Andrea Johns, Alan Hsu, Philip Hansbro, Steven Maltby
2019 Kaiko GE, Chen F, Lai C-W, Chiang I-L, Perrigoue J, Stojmirovic A, et al., 'PAI-1 augments mucosal damage in colitis', SCIENCE TRANSLATIONAL MEDICINE, 11 (2019) [C1]
DOI 10.1126/scitranslmed.aat0852
Citations Scopus - 15Web of Science - 13
Co-authors Bridie Goggins, Paul Foster, Gerard Kaiko
2018 Turner A, Veysey M, Keely S, Scarlett C, Lucock M, Beckett EL, 'Interactions between Bitter Taste, Diet and Dysbiosis: Consequences for Appetite and Obesity.', Nutrients, 10 (2018) [C1]
DOI 10.3390/nu10101336
Citations Scopus - 11Web of Science - 10
Co-authors Emma Beckett, Mark Lucock, C Scarlett, Martin Veysey
2018 Potter MDE, Walker MM, Jones MP, Koloski NA, Keely S, Talley NJ, 'Wheat Intolerance and Chronic Gastrointestinal Symptoms in an Australian Population-based Study: Association Between Wheat Sensitivity, Celiac Disease and Functional Gastrointestinal Disorders', American Journal of Gastroenterology, 113 1036-1044 (2018) [C1]

OBJECTIVES: Wheat avoidance in the absence of celiac disease (CD) is common but occurrence of concurrent functional gastrointestinal disorders (FGIDs) in this group is uncertain. ... [more]

OBJECTIVES: Wheat avoidance in the absence of celiac disease (CD) is common but occurrence of concurrent functional gastrointestinal disorders (FGIDs) in this group is uncertain. The aims of this study were to determine the prevalence of self-reported wheat or gluten sensitivity and doctor diagnosed CD in an Australian population, define the associated gastrointestinal (GI) symptoms and FGIDs, and determine the relationship between self-reported wheat sensitivity, demographic and medical factors. Methods: A total of 3542 people randomly selected from the Australian population returned a mail survey which contained questions on wheat avoidance, GI symptoms, demographic, medical, and lifestyle factors. We defined self-reported wheat sensitivity as people who reported gastrointestinal symptoms on ingestion of wheat based foods, but did not suffer from celiac disease, inflammatory bowel disease or colorectal cancer. Functional dyspepsia (FD) and irritable bowel syndrome (IBS) were diagnosed by Rome III criteria. CD status was self-reported. Results: The prevalence of self-reported wheat sensitivity in this cohort was 14.9% (95% CI 13.7¿16.2). The prevalence of CD was 1.2% (95%CI 0.8¿1.6). Doctor diagnosed CD was significantly associated with a diagnosis of FD (OR 3.35, 95%CI 1.72¿6.52) and IBS (OR 2.28, 95%CI 1.08¿4.81). Those with self-reported wheat sensitivity were more likely to report multiple abdominal symptoms (of the 18 assessed) than those without (3.9 symptoms with self-reported wheat sensitivity vs. 1.6 without, p = 0.0001). In a multivariate analysis, self-reported wheat sensitivity was independently associated with IBS (OR 3.55, 95%CI 2.71¿4.65) and FD (1.48, 95%CI 1.13¿1.94). Conclusions: Self-reported wheat sensitivity is common, with a prevalence of 14.9% in this cohort. There is a strong association between both celiac disease and self-reported wheat sensitivity, and chronic gastrointestinal symptoms, as well as a diagnosis of FD and IBS.

DOI 10.1038/s41395-018-0095-7
Citations Scopus - 31Web of Science - 27
Co-authors Nicholas Talley, Marjorie Walker
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]

Inflammatory bowel disease (IBD) is associated with several immune-mediated extraintestinal manifestations. More than half of all IBD patients have some form of respiratory pathol... [more]

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 - 13Web of Science - 15
Co-authors Bridie Goggins, Hock Tay, Michael Fricker, Steven Maltby, Paul Foster, Andrea Johns, Philip Hansbro, Robert Callister, Jay Horvat, Marjorie Walker
2018 Keely S, Talley NJ, 'Endophenotyping eosinophilic oesophagitis: a new era for management?', LANCET GASTROENTEROLOGY & HEPATOLOGY, 3 449-450 (2018)
DOI 10.1016/S2468-1253(18)30134-1
Co-authors Nicholas Talley
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 - 41Web of Science - 41
Co-authors Bridie Goggins, Michael Fricker, Nicholas Talley, Marjorie Walker, Philip Hansbro
2018 Potter MD, Walker MM, Jones MP, Koloski NA, Keely S, Talley NJ, 'Letter: gluten sensitivity in patients with inflammatory bowel disease', ALIMENTARY PHARMACOLOGY & THERAPEUTICS, 48 1167-1168 (2018)
DOI 10.1111/apt.15012
Co-authors Nicholas Talley, Marjorie Walker
2018 Hollins SL, Brock L, Barreto R, Harms L, Dunn A, Garcia-Sobrinho P, et al., 'A rodent model of anxiety: The effect of perinatal immune challenges on gastrointestinal inflammation and integrity', NeuroImmunoModulation, 25 163-175 (2018) [C1]

Objectives: Gastrointestinal (GI) inflammation and GI integrity deficits are common comorbidities of neuropsychiatric disorders. Ongoing research suggests that these aberrations m... [more]

Objectives: Gastrointestinal (GI) inflammation and GI integrity deficits are common comorbidities of neuropsychiatric disorders. Ongoing research suggests that these aberrations may be contributing to heightened immune signals that have the potential to disrupt neuronal homeostasis and exacerbate behavioural deficits. The current study aimed to determine whether the well-characterized animal model of neuropsychopathology, the maternal immune activation (MIA) model, produced GI inflammation and integrity disruptions in association with anxiety-like behaviour. Methods: Pregnant Wistar rats were exposed to the viral mimetic polyriboinosinic:polyribocytidilic acid (polyI:C) on gestational days (GD) 10 and 19. Evidence of ANS activation, GI inflammation, and GI barrier integrity was assessed in both neonatal (postnatal day, P7) and adult (P84) offspring. Anxiety-like behaviour was assessed at P100. Results: Neonatal MIA offspring exhibited an altered intestinal inflammatory profile and evidence of an increase in lymphoid aggregates. MIA neonates also displayed disruptions to GI barrier tight junction protein mRNA. In addition, adult MIA offspring exhibited an increase in anxiety-like behaviours. Conclusion: These results indicate that the MIA rat model, which is well documented to produce behavioural, neurochemical, and neuroanatomical abnormalities, also produces GI inflammation and integrity disruptions. We suggest that this model may be a useful tool to elucidate biological pathways associated with neuropsychiatric disorders.

DOI 10.1159/000493320
Co-authors Lauren Harms, Deborah Hodgson, Marjorie Walker, Phil Dickson
2018 McIlroy DJ, Minahan K, Keely S, Lott N, Hansbro P, Smith DW, Balogh ZJ, 'Reduced deoxyribonuclease enzyme activity in response to high postinjury mitochondrial DNA concentration provides a therapeutic target for Systemic Inflammatory Response Syndrome.', J Trauma Acute Care Surg, 85 354-358 (2018) [C1]
DOI 10.1097/TA.0000000000001919
Citations Scopus - 9Web of Science - 8
Co-authors Douglas Smith, Zsolt Balogh
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]

The intestinal epithelium constitutes an innate barrier which, upon injury, undergoes self-repair processes known as restitution. Although bile acids are known as important regula... [more]

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 T 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- -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. 84 inh -

DOI 10.1152/ajpgi.00435.2016
Citations Scopus - 16Web of Science - 14
Co-authors Bridie Goggins
2018 Potter MDE, Walker MM, Keely S, Talley NJ, 'What's in a name? 'Non-coeliac gluten or wheat sensitivity': controversies and mechanisms related to wheat and gluten causing gastrointestinal symptoms or disease.', Gut, 67 2073-2077 (2018) [C1]
DOI 10.1136/gutjnl-2018-316360
Citations Scopus - 10Web of Science - 7
Co-authors Marjorie Walker, Nicholas Talley
2017 Farrell KE, Keely S, Walker MM, Brichta AM, Graham BA, Callister RJ, 'Altered intrinsic and synaptic properties of lumbosacral dorsal horn neurons in a mouse model of colitis', Neuroscience, 362 152-167 (2017) [C1]

Visceral pain in inflammatory and functional gastrointestinal conditions is a major clinical problem. The exact mechanisms underlying the development of pain, during and after vis... [more]

Visceral pain in inflammatory and functional gastrointestinal conditions is a major clinical problem. The exact mechanisms underlying the development of pain, during and after visceral inflammation are unknown. However, clinical and pre-clinical evidence suggests plasticity within the spinal cord dorsal horn is a contributing factor. Here we use an in vivo preparation and patch-clamp electrophysiology to test whether the synaptic and intrinsic properties of superficial dorsal horn (SDH) neurons are altered 5 days after the induction of mild colitis in adult male mice (i.e. during acute inflammation of the colon). Whole-cell recordings were made from lumbosacral (L6-S1) superficial dorsal horn neurons (SDH), in animals under isoflurane anesthesia. Noxious colorectal distension (CRD) was used to identify SDH neurons with colonic inputs, while stimulation of the hind paw and tail was employed to assess convergent cutaneous input. Following inflammation, a significantly increased proportion of SDH neurons received both colonic and cutaneous inputs, compared to neurons in naïve animals. In addition, the nature and magnitude of responses to CRD and cutaneous stimulation differed in inflamed animals, as was spontaneous excitatory synaptic drive. Conversely, several measures of intrinsic excitability were altered in a manner that would decrease SDH network excitability following colitis. We propose that during inflammation, sensitization of colonic afferents results in increased signaling to the SDH. This is accompanied by plasticity in SDH neurons whereby their intrinsic properties are changed to compensate for altered afferent activity.

DOI 10.1016/j.neuroscience.2017.08.029
Citations Scopus - 2Web of Science - 2
Co-authors Robert Callister, Alan Brichta, Marjorie Walker, Brett Graham
2017 Ward JBJ, Lajczak NK, Kelly OB, O Dwyer AM, Giddam AK, Ní Gabhann J, et al., 'Ursodeoxycholic acid and lithocholic acid exert anti-inflammatory actions in the colon', American Journal of Physiology - Gastrointestinal and Liver Physiology, 312 G550-G558 (2017) [C1]

Inflammatory bowel diseases (IBD) comprise a group of common and debilitating chronic intestinal disorders for which currently available therapies are often unsatisfactory. The na... [more]

Inflammatory bowel diseases (IBD) comprise a group of common and debilitating chronic intestinal disorders for which currently available therapies are often unsatisfactory. The naturally occurring secondary bile acid, ursodeoxycholic acid (UDCA), has well-established anti-inflammatory and cytoprotective actions and may therefore be effective in treating IBD. We aimed to investigate regulation of colonic inflammatory responses by UDCA and to determine the potential impact of bacterial metabolism on its therapeutic actions. The anti-inflammatory efficacy of UDCA, a nonmetabolizable analog, 6a-methyl-UDCA (6-MUDCA), and its primary colonic metabolite lithocholic acid (LCA) was assessed in the murine dextran sodium sulfate (DSS) model of mucosal injury. The effects of bile acids on cytokine (TNF-a, IL-6, Il-1ß, and IFN-¿) release from cultured colonic epithelial cells and mouse colonic tissue in vivo were investigated. Luminal bile acids were measured by gas chromatography-mass spectrometry. UDCA attenuated release of proinflammatory cytokines from colonic epithelial cells in vitro and was protective against the development of colonic inflammation in vivo. In contrast, although 6-MUDCA mimicked the effects of UDCA on epithelial cytokine release in vitro, it was ineffective in preventing inflammation in the DSS model. In UDCA-treated mice, LCA became the most common colonic bile acid. Finally, LCA treatment more potently inhibited epithelial cytokine release and protected against DSS-induced mucosal inflammation than did UDCA. These studies identify a new role for the primary metabolite of UDCA, LCA, in preventing colonic inflammation and suggest that microbial metabolism of UDCA is necessary for the full expression of its protective actions. NEW & NOTEWORTHY On the basis of its cytoprotective and anti-inflammatory actions, the secondary bile acid ursodeoxycholic acid (UDCA) has well-established uses in both traditional and Western medicine. We identify a new role for the primary metabolite of UDCA, lithocholic acid, as a potent inhibitor of intestinal inflammatory responses, and we present data to suggest that microbial metabolism of UDCA is necessary for the full expression of its protective effects against colonic inflammation.

DOI 10.1152/ajpgi.00256.2016
Citations Scopus - 53Web of Science - 49
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 - 95Web of Science - 99
Co-authors Joerg Mattes, Paul Foster, Nicole Hansbro, Philip Hansbro, Malcolm Starkey, Jay Horvat, Jemma Mayall
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 - 13Web of Science - 13
Co-authors Martin Veysey, Nicholas Talley, Robert Callister, Paul Foster, Bridie Goggins, Marjorie Walker
2016 Walker MM, Keely SJ, Scott RJ, Talley NJ, 'Genetics, Mucosal Inflammation and the Environment in Post-Infectious Chronic Gut Syndromes', The American Journal of Gastroenterology Supplements, 3 46-51 (2016) [C1]
DOI 10.1038/ajgsup.2016.14
Co-authors Nicholas Talley, Marjorie Walker, Rodney Scott
2016 Farrell KE, Rank MM, Keely S, Brichta AM, Graham BA, Callister RJ, 'In vivo characterization of colorectal and cutaneous inputs to lumbosacral dorsal horn neurons in the mouse spinal cord', Neuroscience, 316 13-25 (2016) [C1]

Chronic abdominal pain is a common symptom of inflammatory bowel disease and often persists in the absence of gut inflammation. Although the mechanisms responsible for ongoing pai... [more]

Chronic abdominal pain is a common symptom of inflammatory bowel disease and often persists in the absence of gut inflammation. Although the mechanisms responsible for ongoing pain are unknown, clinical and preclinical evidence suggests lumbosacral spinal cord dorsal horn neurons contribute to these symptoms. At present, we know little about the intrinsic and synaptic properties of this population of neurons in either normal or inflammed conditions. Therefore, we developed an in vivo preparation to make patch-clamp recordings from superficial dorsal horn (SDH) neurons receiving colonic inputs in naïve male mice. Recordings were made in the lumbosacral spinal cord (L6-S1) under isoflurane anesthesia. Noxious colorectal distension (CRD) was used to determine whether SDH neurons received inputs from mechanical stimulation/distension of the colon. Responses to hind paw/tail cutaneous stimulation and intrinsic and synaptic properties were also assessed, as well as action potential discharge properties. Approximately 11% of lumbosacral SDH neurons in the cohort of neurons sampled responded to CRD and a majority of these responses were subthreshold. Most CRD-responsive neurons (80%) also responded to cutaneous stimuli, compared with <50% of CRD-non-responsive neurons. Furthermore, CRD-responsive neurons had more hyperpolarized resting membrane potentials, larger rheobase currents, and reduced levels of excitatory drive, compared to CRD-non-responsive neurons. Our results demonstrate that CRD-responsive neurons can be distinguished from CRD-non-responsive neurons by several differences in their membrane properties and excitatory synaptic inputs. We also demonstrate that SDH neurons with colonic inputs show predominately subthreshold responses to CRD and exhibit a high degree of viscerosomatic convergence.

DOI 10.1016/j.neuroscience.2015.12.023
Citations Scopus - 6Web of Science - 6
Co-authors Michelle Rank, Robert Callister, Alan Brichta, Brett Graham
2016 Cuív P, Begun J, Keely S, Lewindon PJ, Morrison M, 'Towards an integrated understanding of the therapeutic utility of exclusive enteral nutrition in the treatment of Crohn's disease', Food and Function, 7 1741-1751 (2016) [C1]

Crohn&apos;s disease (CD) is a chronic disease characterized by episodic and disabling inflammation of the gastrointestinal tract in genetically susceptible individuals. The incid... [more]

Crohn's disease (CD) is a chronic disease characterized by episodic and disabling inflammation of the gastrointestinal tract in genetically susceptible individuals. The incidence and prevalence of CD is rising rapidly across the world emphasising that disease risk is also influenced by environmental and lifestyle factors, as well as the microbial community resident in the gut. Childhood-onset CD is associated with an aggressive disease course that can adversely impact patient growth and development. There is no cure for CD however new onset and recurrent cases of paediatric CD are often responsive to exclusive enteral nutrition (EEN) treatment. EEN treatment involves the exclusive consumption of an elemental or polymeric formula for several weeks and it is well established as a primary intervention strategy. EEN treatments typically achieve remission rates of over 80% and importantly they are associated with a high rate of mucosal healing, far superior to steroids, which is prognostic of improved long-term health outcomes. Furthermore, they are safe, have few side effects, and improve nutritional status and linear growth. Surprisingly, despite the utility of EEN our understanding of the host-microbe-diet interactions that underpin clinical remission and mucosal healing are limited. Here, we review the current state of knowledge and propose that the induction of autophagy, in addition to modulation of the microbiota and coordinated effects on inflammation and epithelial cell biology, may be critical for the therapeutic effects associated with EEN. A better understanding of EEN treatment will provide new opportunities to restore gut homeostasis and prolong periods of remission, as well as provide new insights into the factors that trigger and perhaps prevent CD.

DOI 10.1039/c5fo01196e
Citations Scopus - 9Web of Science - 9
2016 Mateer SW, Cardona J, Marks E, Goggin BJ, Hua S, Keely S, 'Ex Vivo Intestinal Sacs to Assess Mucosal Permeability in Models of Gastrointestinal Disease.', J Vis Exp, e53250 (2016) [C1]
DOI 10.3791/53250
Citations Scopus - 16Web of Science - 13
Co-authors Susan Hua
2015 Hua S, Marks E, Schneider JJ, Keely S, 'Advances in oral nano-delivery systems for colon targeted drug delivery in inflammatory bowel disease: selective targeting to diseased versus healthy tissue.', Nanomedicine, 11 1117-1132 (2015) [C1]
DOI 10.1016/j.nano.2015.02.018
Citations Scopus - 214Web of Science - 199
Co-authors Jennifer Schneider, Susan Hua
2015 Keely S, Walker MM, Marks E, Talley NJ, 'Immune dysregulation in the functional gastrointestinal disorders', European Journal of Clinical Investigation, 45 1350-1359 (2015) [C1]
DOI 10.1111/eci.12548
Citations Scopus - 51Web of Science - 49
Co-authors Nicholas Talley, Marjorie Walker
2015 Keely S, Veysey M, Walker MM, Talley NJ, 'Letter: oxidative stress, cause or consequence of constipation-associated colorectal cancer?', Aliment Pharmacol Ther, 42 941-942 (2015) [C3]
DOI 10.1111/apt.13349
Co-authors Nicholas Talley, Marjorie Walker, Martin Veysey
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 - 30Web of Science - 30
Co-authors Bridie Goggins, Marjorie Walker
2015 Keely S, Foster PS, 'Stop Press: Eosinophils Drafted to Join the Th17 Team', IMMUNITY, 43 7-9 (2015) [C3]
DOI 10.1016/j.immuni.2015.07.010
Citations Scopus - 13Web of Science - 11
Co-authors Paul Foster
2014 Keely S, Hansbro PM, 'Lung-Gut Cross Talk A Potential Mechanism for Intestinal Dysfunction in Patients With COPD', CHEST, 145 199-200 (2014) [C3]
DOI 10.1378/chest.13-2077
Citations Scopus - 21Web of Science - 18
Co-authors Philip Hansbro
2014 Ward JBJ, Keely SJ, Keely SJ, 'Oxygen in the regulation of intestinal epithelial transport', Journal of Physiology, 592 2473-2489 (2014) [C1]

The transport of fluid, nutrients and electrolytes to and from the intestinal lumen is a primary function of epithelial cells. Normally, the intestine absorbs approximately 9 l of... [more]

The transport of fluid, nutrients and electrolytes to and from the intestinal lumen is a primary function of epithelial cells. Normally, the intestine absorbs approximately 9 l of fluid and 1 kg of nutrients daily, driven by epithelial transport processes that consume large amounts of cellular energy and O . The epithelium exists at the interface of the richly vascularised mucosa, and the anoxic luminal environment and this steep O gradient play a key role in determining the expression pattern of proteins involved in fluid, nutrient and electrolyte transport. However, the dynamic nature of the splanchnic circulation necessitates that the epithelium can evoke co-ordinated responses to fluctuations in O availability, which occur either as a part of the normal digestive process or as a consequence of several pathophysiological conditions. While it is known that hypoxia-responsive signals, such as reactive oxygen species, AMP-activated kinase, hypoxia-inducible factors, and prolyl hydroxylases are all important in regulating epithelial responses to altered O supply, our understanding of the molecular mechanisms involved is still limited. Here, we aim to review the current literature regarding the role that O plays in regulating intestinal transport processes and to highlight areas of research that still need to be addressed. © 2014 The Physiological Society. 2 2 2 2 2

DOI 10.1113/jphysiol.2013.270249
Citations Scopus - 28Web of Science - 23
2014 Farrell KE, Keely S, Graham BA, Callister R, Callister RJ, 'A Systematic Review of the Evidence for Central Nervous System Plasticity in Animal Models of Inflammatory-mediated Gastrointestinal Pain', INFLAMMATORY BOWEL DISEASES, 20 176-195 (2014) [C1]
DOI 10.1097/01.MIB.0000437499.52922.b1
Citations Scopus - 27Web of Science - 23
Co-authors Robin Callister, Brett Graham, Robert Callister
2014 Farrell KE, Callister RJ, Keely S, 'Understanding and targeting centrally mediated visceral pain in inflammatory bowel disease', Frontiers in Pharmacology, 5 1-4 (2014) [C3]
DOI 10.3389/fphar.2014.00027
Citations Scopus - 16Web of Science - 13
Co-authors Robert Callister
2014 Keely S, Campbell EL, Baird AW, Hansbro PM, Shalwitz RA, Kotsakis A, et al., 'Contribution of epithelial innate immunity to systemic protection afforded by prolyl hydroxylase inhibition in murine colitis', Mucosal Immunology, 7 114-123 (2014) [C1]

Pharmacological stabilization of hypoxia-inducible factor (HIF) through prolyl hydroxylase (PHD) inhibition limits mucosal damage associated with models of murine colitis. However... [more]

Pharmacological stabilization of hypoxia-inducible factor (HIF) through prolyl hydroxylase (PHD) inhibition limits mucosal damage associated with models of murine colitis. However, little is known about how PHD inhibitors (PHDi) influence systemic immune function during mucosal inflammation or the relative importance of immunological changes to mucosal protection. We hypothesized that PHDi enhances systemic innate immune responses to colitis-associated bacteremia. Mice with colitis induced by trinitrobenzene sulfonic acid were treated with AKB-4924, a new HIF-1 isoform-predominant PHDi, and clinical, immunological, and biochemical endpoints were assessed. Administration of AKB-4924 led to significantly reduced weight loss and disease activity compared with vehicle controls. Treated groups were pyrexic but did not become subsequently hypothermic. PHDi treatment augmented epithelial barrier function and led to an approximately 50-fold reduction in serum endotoxin during colitis. AKB-4924 also decreased cytokines involved in pyrogenesis and hypothermia, significantly reducing serum levels of interleukin (IL)-1ß, IL-6, and tumor necrosis factor (TNF)-a while increasing IL-10. Treatment offered no protection against colitis in epithelial-specific HIF-1a-deficient mice, strongly implicating epithelial HIF-1a as the tissue target for AKB-4924-mediated protection. Taken together, these results indicate that inhibition of prolyl hydroxylase with AKB-4924 enhances innate immunity and identifies that the epithelium is a central site of inflammatory protection afforded by PHDi in murine colitis. © 2014 Society for Mucosal Immunology.

DOI 10.1038/mi.2013.29
Citations Scopus - 69Web of Science - 70
Co-authors Philip Hansbro
2014 Goggins B, Minahan K, Kostakis A, Shalwitz R, Horvat J, Keely S, 'Stabilisation of epithelial hypoxia-inducible factor reverses colitis through accelerated restitution', FASEB JOURNAL, 28 (2014)
Co-authors Jay Horvat
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 - 35Web of Science - 34
Co-authors Jay Horvat, Bridie Goggins
2013 Hansbro P, Beckett E, Stevens R, Jarnicki A, Wark P, Foster P, 'A short-term model of COPD identifies a role for mast cell tryptase', EUROPEAN RESPIRATORY JOURNAL, 42 (2013) [C3]
Co-authors Peter Wark, Jay Horvat, Philip Hansbro, Paul Foster
2013 Beckett EL, Stevens RL, Jarnicki AG, Kim RY, Hanish I, Hansbro NG, et al., 'A new short-term mouse model of chronic obstructive pulmonary disease identifies a role for mast cell tryptase in pathogenesis', The Journal of Allergy and Clinical Immunology, 131 752-762 (2013) [C1]
Citations Scopus - 132Web of Science - 134
Co-authors Peter Wark, Emma Beckett, Jay Horvat, Nicole Hansbro, Philip Hansbro, Ming Yang, Paul Foster
2012 Keely S, Kelly C, Weissmueller T, Burgess A, Wagner B, Robertson CE, et al., 'Activated fluid transport regulates bacterial-epithelial interactions and significantly shifts the murine colonic microbiome', Gut Microbes, 3 250-260 (2012) [C1]
DOI 10.4161/gmic.20529
Citations Scopus - 37Web of Science - 34
2012 Keely S, Talley NJ, Hansbro PM, 'Pulmonary-intestinal cross-talk in mucosal inflammatory disease', Mucosal Immunology, 5 7-18 (2012) [C1]
DOI 10.1038/mi.2011.55
Citations Scopus - 140Web of Science - 134
Co-authors Nicholas Talley, Philip Hansbro
2011 Macmanus C, Campbell E, Keely S, Adrienne B, Kominsky D, Colgan S, 'Anti-inflammatory actions of adrenomedullin through fine tuning of HIF stabilization', The FASEB Journal, 25 1856-1864 (2011) [C1]
DOI 10.1096/fj.10-170316
Citations Scopus - 31Web of Science - 31
2011 Keely S, Feighery L, Campion DP, O'Brien L, Brayden DJ, Baird AW, 'Chloride-led disruption of the intestinal mucous layer impedes salmonella invasion: Evidence for an 'enteric tear' mechanism', Cellular Physiology and Biochemistry, 28 743-752 (2011) [C1]
DOI 10.1159/000335768
Citations Scopus - 12Web of Science - 10
2011 Kominsky D, Keely S, Macmanus C, Glover L, Scully M, Collins C, et al., 'An Endogenously Anti-Inflammatory Role for Methylation in Mucosal Inflammation Identified through Metabolite Profiling.', Journal of Immunology, 186 6505-6514 (2011) [C1]
DOI 10.4049/jimmunol.1002805
Citations Scopus - 47Web of Science - 42
2010 Campbell E, Macmanus C, Kominsky D, Keely S, Glover L, Scully M, et al., 'Resolvin E1-induced Intestinal Alkaline Phosphatase Promotes Resolution of Inflammation through LPS detoxification.', Proceedings of the National Academy of Sciences of USA, 107 4298-4303 (2010) [C1]
DOI 10.1073/pnas.0914730107
Citations Scopus - 126Web of Science - 120
2010 Keely S, Glover L, Weissmueller T, Macmanus C, Fillon S, Fennimore B, Colgan S, 'Hypoxia-inducible factor-dependent regulation of platelet-activating factor receptor as a route for gram-positive bacterial translocation across epithelia', Molecular Biology of the Cell, 21 538-546 (2010) [C1]
DOI 10.1091/mbc.E09-07-0573
Citations Scopus - 39Web of Science - 36
2009 Keely S, Ryan S, Haddleton D, Limer A, Mantovani G, Murphy E, Brayden D, 'Dexamethasone-pDMAEMA polymeric conjugates reduce inflammatory biomarkers in human intestinal epithelial monolayers.', Journal of Controlled Release, 135 35-43 (2009) [C1]
DOI 10.1016/j.jconrel.2008.12.001
Citations Scopus - 32Web of Science - 32
2009 Keely S, Glover L, Macmanus C, Campbell E, Scully M, Furuta G, Colgan S, 'Selective induction of integrin beta1 by hypoxia-inducible factor: implications for wound healing.', The FASEB Journal, 23 1338-1346 (2009) [C1]
DOI 10.1096/fj.08-125344
Citations Scopus - 67Web of Science - 70
2008 Robinson A, Keely S, Karhausen J, Gerich M, Furuta G, Colgan S, 'Mucosal protection by hypoxia-inducible factor prolyl hydroxylase inhibition.', Gastroenterology, 134 346-348 (2008) [C1]
DOI 10.1053/j.gastro.2007.09.033
Citations Scopus - 272Web of Science - 274
2008 Feighery L, Smyth A, Keely S, Baird A, O'Connor W, Callanan J, Brayden D, 'Increased intestinal permeability in rats subjected to traumatic frontal lobe percussion brain injury.', Journal of Trauma: Injury Infection and Critical Care, 64 131-137 (2008) [C1]
DOI 10.1097/TA.0b013e3181568d9f
Citations Scopus - 33Web of Science - 35
2008 Boland T, Hayes L, Sweeney T, Callanan J, Baird A, Keely S, Crosby T, 'The effects of cobalt and iodine supplementation of the pregnant ewe diet on immunoglobulin G, vitamin E, T-3 and T-4 levels in the progeny.', Animal: the international journal of animal biosciences, 2 197-206 (2008) [C1]
DOI 10.1017/S175173110700105X
Citations Scopus - 17Web of Science - 16
2008 Fanning R, Campion D, Collins C, Keely S, Briggs L, O'Connor J, Carey M, 'A comparison of the inhibitory effects of bupivacaine and levobupivacaine on isolated human pregnant myometrium contractility.', Anesthesia and Analgesia, 107 1303-1307 (2008) [C1]
DOI 10.1213/ane.0b013e3181804245
Citations Scopus - 12Web of Science - 10
2008 Keely S, Rawlinson L-AB, Haddleton DM, Brayden DJ, 'A tertiary amino-containing polymethacrylate polymer protects mucus-covered intestinal epithelial monolayers against pathogenic challenge', Pharmaceutical Research, 25 1193-1201 (2008) [C1]
DOI 10.1007/s11095-007-9501-3
Citations Scopus - 12Web of Science - 12
2006 Limer A, Attvinder R, San Miguel V, Peinado C, Keely S, Fitzpatrick E, et al., 'Fluorescently tagged star polymers by living radical polymerisation for mucoadhesion and bioadhesion.', Reactive and Functional Polymers, 66 51-64 (2006) [C1]
DOI 10.1016/j.reactfunctpolym.2005.07.024
Citations Scopus - 57Web of Science - 52
2005 Keely S, Atvinder R, Wilson C, Carmichael A, Carrington S, Corfield A, et al., 'In vitro and ex vivo intestinal tissue models to measure mucoadhesion of poly (methacrylate) and N-trimethylated chitosan polymers.', Pharmaceutical Research, 22 38-49 (2005) [C1]
DOI 10.1007/s11095-004-9007-1
Citations Scopus - 72Web of Science - 68
Show 82 more journal articles

Review (1 outputs)

Year Citation Altmetrics Link
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 (2015) [C1]
DOI 10.1189/jlb.3RU1114-563R
Citations Scopus - 16Web of Science - 16
Co-authors Jay Horvat, Paul Foster, Steven Maltby, Philip Hansbro

Conference (49 outputs)

Year Citation Altmetrics Link
2020 Goggins B, Minahan K, Sherwin S, Liu G, Walker M, Horvat J, et al., 'Hypoxia Inducible Factor (HIF)-1 accelerates mucosal wound healing through regulation and trafficking of integrin-alpha 5 beta 1', FASEB JOURNAL, San Diego, CA (2020)
DOI 10.1096/fasebj.2020.34.s1.07414
Co-authors Jay Horvat, Darryl Knight, Bridie Goggins, Marjorie Walker
2020 Shah A, Talley N, Kang S, Anh D, Walker M, Koloski N, et al., 'Self-reported non-celiac wheat sensitivity (NCWS) in patients with chronic unexplained (functional) gastrointestinal symptoms', NEUROGASTROENTEROLOGY AND MOTILITY (2020)
Co-authors Marjorie Walker, Nicholas Talley
2020 Shah A, Talley N, Koloski N, Shanahan E, Walker M, Keely S, et al., 'Quantitative PCR as a novel approach to determine small intestinal bacterial load in health and disease', NEUROGASTROENTEROLOGY AND MOTILITY (2020)
Co-authors Marjorie Walker, Nicholas Talley
2020 Potter MD, Duncanson K, Burns G, Walker MM, Keely S, Talley NJ, 'FUNCTIONAL DYSPEPSIA AND NON-CELIAC WHEAT SENSITIVITY: RESULTS FROM A PILOT DOUBLE BLIND, PLACEBO CONTROLLED, DIETARY CROSSOVER TRIAL', GASTROENTEROLOGY, Austin, TX (2020)
Co-authors Nicholas Talley, Kerith Duncanson, Marjorie Walker
2019 Liu G, Mateer S, Hsu A, Goggins B, Tay H, Mathe A, et al., 'Platelet activating factor receptor regulates colitis-induced pulmonary inflammation through the NLRP3 inflammasome', EUROPEAN JOURNAL OF IMMUNOLOGY, Beijing, PEOPLES R CHINA (2019)
Co-authors Alan Hsu, Philip Hansbro, Hock Tay, Steven Maltby, Andrea Johns, Michael Fricker
2018 Talley NJ, Holtmann G, Walker MM, Jones M, Koloski NA, Keely S, 'Anti-Cytolethal Distending Toxin B Antibody (Anti-CdtB) Differentiates Functional Dyspepsia From Healthy Controls', AMERICAN JOURNAL OF GASTROENTEROLOGY, Philadelphia, PA (2018)
Co-authors Nicholas Talley, Marjorie Walker
2018 Talley NJ, Holtmann G, Walker MM, Jones M, Koloski NA, Keely S, 'Zonulin as a Biomarker to Identify the Irritable Bowel Syndrome (IBS), Functional Dyspepsia (FD), and Non-Celiac Wheat Sensitivity (NCWS)', AMERICAN JOURNAL OF GASTROENTEROLOGY, Philadelphia, PA (2018)
Co-authors Marjorie Walker, Nicholas Talley
2018 Liu G, Mateer S, Mathe A, Goggins B, Hsu A, Minahan K, et al., 'Platelet Activating Factor Receptor (PAFR) Regulates Colitis-induced Pulmonary Inflammation', FASEB JOURNAL, Amer Assoc Anatomists, San Diego, CA (2018)
Co-authors Philip Hansbro, Michael Fricker, Alan Hsu, Peter Wark, Andrea Johns
2018 Potter MD, Jones MP, Koloski NA, Keely S, Walker MM, Talley NJ, 'Non-celiac wheat sensitivity and celiac disease are strongly and independently associated with inflammatory bowel disease: A population-based study of 3542 randomly selected people', JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY (2018)
Citations Web of Science - 1
Co-authors Nicholas Talley, Marjorie Walker
2018 Shah A, Shanahan E, Berendsen E, Macdonald G, Rich J, Ghasemi P, et al., 'Quantitative polymerase chain reaction as a novel approach to determine influence of density of bacterial colonization on health and disease', JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY (2018)
Co-authors Nicholas Talley
2018 Holtmann G, Do A, Walker MM, Shah A, Shanahan E, Morrison M, et al., 'Non-celiac wheat sensitivity and small intestinal mucosal immune activation are associated with specific alterations in small intestinal mucosa-associated microbiome', JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY (2018)
Co-authors Nicholas Talley, Marjorie Walker
2018 Koloski NA, Jones MP, Walker MM, Veysey M, Alkesh Z, Keely S, et al., 'UNDERSTANDING THE INTERRELATIONSHIPS BETWEEN SLEEP DISTURBANCE, PSYCHOLOGICAL DISTRESS AND FUNCTIONAL GASTROINTESTINAL DISORDERS. A POPULATION-BASED STUDY OF 3542 AUSTRALIANS', GASTROENTEROLOGY, Washington, DC (2018)
Co-authors Nicholas Talley, Marjorie Walker, Martin Veysey
2018 Koloski NA, Jones MP, Walker MM, Veysey M, Alkesh Z, Keely S, et al., 'ATOPY AND AUTOIMMUNE DISEASES ARE LINKED TO PSYCHOLOGICAL DISTRESS VIA THE PRESENCE OF FUNCTIONAL GASTROINTESTINAL DISORDERS. A POPULATION-BASED STUDY OF 3542 AUSTRALIANS', GASTROENTEROLOGY, Washington, DC (2018)
Co-authors Martin Veysey, Nicholas Talley, Marjorie Walker
2017 Anh D, Shanahan ER, Shah A, Ghasemi P, Hansen T, Koloski N, et al., 'Mucosa-associated microbiota and specific peripheral T-cell populations modulate gut-homing integrin a4&b7', JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY (2017)
Co-authors Nicholas Talley, Marjorie Walker
2017 Shanahan ER, Shah A, Do A, Ghasemi P, Hansen T, Koloski N, et al., 'Cigarette smoking and diversity of the duodenal mucosa associated microbiome', JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY (2017)
Citations Web of Science - 1
Co-authors Marjorie Walker, Nicholas Talley
2017 Mathe A, Zierau O, Keely S, 'Can Hormonal Changes Influence DNA Integrity to Protect us from Colorectal Cancer?', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2017)
Co-authors Andrea Johns
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 Jay Horvat, Bridie Goggins, Darryl Knight
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 Bridie Goggins
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 Nicholas Talley, Bridie Goggins, Marjorie Walker, Paul Foster, Robert Callister, Martin Veysey
2017 Potter M, Walker MM, Jones M, Koloski N, Brogan G, Keely S, Talley N, 'Functional Dyspepsia Symptoms Are Strongly Associated With Coeliac Disease: Results From a Population-Based Study', AMERICAN JOURNAL OF GASTROENTEROLOGY, Orlando, FL (2017)
DOI 10.14309/00000434-201710001-00463
Co-authors Nicholas Talley, Marjorie Walker
2016 Horvat J, Kim R, Pinkerton J, Rae B, Starkey M, Essilfie A, et al., 'IDENTIFICATION OF NOVEL THERAPEUTIC TARGETS FOR STEROID-INSENSITIVE ASTHMA USING MODELS THAT REPRESENT DIFFERENT CLINICAL SUBTYPES OF DISEASE', RESPIROLOGY (2016)
Co-authors Jay Horvat, Philip Hansbro, Joerg Mattes
2016 Gellatly S, Dennis P, Jarnicki A, Lachner N, Wood D, Fricker M, et al., 'HEALTHY GUT MICROBIOTA AMELIORATES EXPERIMENTAL CHRONIC OBSTRUCTIVE PULMONARY DISEASE', RESPIROLOGY (2016)
Co-authors Philip Hansbro, Michael Fricker
2016 Horvat J, Kim R, Pinkerton J, Rae B, Starkey M, Essilfie A-T, et al., 'Identification of therapeutic targets for steroid-insensitive asthma using models that represent different clinical subtypes of disease', EUROPEAN RESPIRATORY JOURNAL (2016)
DOI 10.1183/13993003.congress-2016.PA563
Co-authors Philip Hansbro, Paul Foster, Jay Horvat, Joerg Mattes
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, Philip Hansbro, Malcolm Starkey, Jay Horvat, Jemma Mayall, Joerg Mattes
2015 Farrell K, Rank M, Keely S, Graham B, Callister R, 'In vivo electrophysiological characterisation of mouse lumbosacral dorsal horn neurons receiving visceral inputs', JOURNAL OF NEUROCHEMISTRY, Cairns, AUSTRALIA (2015) [E3]
Co-authors Brett Graham, Michelle Rank, Robert Callister
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 Bridie Goggins, Jay Horvat, Philip Hansbro, Steven Maltby
2015 Hansbro P, Kim R, Pinkerton J, Starkey M, Essilfie A-T, Mayall J, et al., 'MicroRNA-21 drives severe, steroid-insensitive experimental asthma by amplifying PI3K-mediated suppression of HDAC2', JOURNAL OF IMMUNOLOGY, New Orleans, LA (2015)
Co-authors Jay Horvat, Joerg Mattes, Paul Foster, Philip Hansbro
2015 Naudin C, Weidenhofer J, Roselli S, Keely S, 'Induction of Mindin is Associated with Pathological Changes in the Kidney of Cd151(-/-) Mice', FASEB JOURNAL (2015) [E3]
Co-authors Severine Roselli, Judith Weidenhofer
2015 Hansbro PM, Kim RY, Pinkerton JW, Starkey MR, Essilfie AT, Mayall JR, et al., 'Infection-Induced Microrna-21 Drives Severe, Steroid-Insensitive Experimental Asthma By Amplifying PhosphoINOSitide-3-Kinase (pi3k)-Mediated Suppression Of Histone Deacetylase (hdac)2', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Denver, CO (2015)
Co-authors Jay Horvat, Joerg Mattes, Paul Foster, Philip Hansbro, Malcolm Starkey
2014 Fricker M, Walker MM, Talley NJ, Keely S, Hansbro P, 'Colon Pathology in a Mouse Model of Cigarette Smoke Induced Chronic Obstructive Pulmonary Disease (COPD) - A Model for Induction of Crohn's Disease?', GASTROENTEROLOGY, Chicago, IL (2014)
Co-authors Nicholas Talley, Michael Fricker, Philip Hansbro, Marjorie Walker
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 Jay Horvat, Bridie Goggins, 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 Bridie Goggins, 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 Bridie Goggins
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 Philip Hansbro, Jay Horvat, Bridie Goggins, Steven Maltby
2014 Farrell KE, Graham BA, Keely S, Callister RJ, 'Understanding the mechanisms underlying chronic pain in IBD: A new method for studying visceral inputs from the gastrointestinal tract', JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY (2014) [E3]
Co-authors Brett Graham, Robert Callister
2014 Aghdam FF, Hsu A, Parsons K, Keely S, Wood L, Wark P, 'Oxidative stress impairs mitochondria], function and leads to deficient antiviral responses in primary bronchial epithelial cells', EUROPEAN RESPIRATORY JOURNAL (2014)
Co-authors Alan Hsu, Lisa Wood, Peter Wark
2014 Aghdam FF, Wood L, Hsu A, Parsons K, Keely S, Wark P, 'Comparing the effects of oxidative stress on mitochondrial function and antiviral responses in primary bronchial epithelial cells of asthmatics and non-asthmatics', EUROPEAN RESPIRATORY JOURNAL (2014)
Co-authors Alan Hsu, Peter Wark, Lisa Wood
2014 Fathi F, Hsu A, Parsons K, Keely S, Wood L, Wark P, 'OXIDATIVE STRESS IMPAIRS MITOCHONDRIAL FUNCTION AND LEADS TO DEFICIENT ANTIVIRAL RESPONSES IN PRIMARY BRONCHIAL EPITHELIAL CELLS', RESPIROLOGY (2014) [E3]
DOI 10.1111/resp.12263_3
Co-authors Lisa Wood, Peter Wark, Alan Hsu
2013 Hansbro P, Beckett E, Stevens R, Jarnicki A, Kim R, Hanish I, et al., 'A short-term model of COPD identifies a role for mast cell tryptase', JOURNAL OF IMMUNOLOGY, Honolulu, HI (2013) [E3]
Co-authors Jay Horvat, Emma Beckett, Peter Wark, Ming Yang, Paul Foster, Nicole Hansbro, Philip Hansbro
2012 Farrell KE, Keely S, Graham BA, Minahan KL, Madden JF, Callister RJ, 'Spinal cord signalling in a mouse model of inflammatory bowel disease', Journal of Gastroenterology and Hepatology, Adelaide, SA (2012) [E3]
Co-authors Brett Graham, Robert Callister
2012 Nolan GM, Minahan KL, Farrell KE, Chaney C, Mateer S, Talley NJ, Keely S, 'Hypoxia-inducible factor-1 a promotes mucosal protection in colitis via the IL-12 signalling pathway', Journal of Gastroenterology and Hepatology, Adelaide, S.A. (2012) [E3]
Co-authors Nicholas Talley
2012 Mateer S, Hansbro PM, Nolan GM, Chaney C, Minahan KL, Keely S, 'Development of pulmonary inflammation and altered lung function in a mouse model of colitis', Journal of Gastroenterology and Hepatology, Adelaide, S.A. (2012) [E3]
Co-authors Philip Hansbro
2012 Keely S, Baird AW, Colgan S, 'Epithelial HIF-1 a is critical to the protective action of prolyl hydroxylase inhibition in a murine model of inflammatory bowel disease', Journal of Gastroenterology and Hepatology, Adelaide, S.A. (2012) [E3]
2012 Chaney C, Minahan KL, Mateer S, Nolan GM, Talley NJ, Keely S, 'Hypoxic regulation of ß1 integrin during mucosal wound healing', Journal of Gastroenterology and Hepatology, Adelaide, S.A. (2012) [E3]
Co-authors Nicholas Talley
2012 Keely S, Baird A, Kominsky D, McNamee EN, Hansbro PM, Shalwitz RA, Colgan SP, 'Immune modulation by prolyl hydroxylase inhibition contributes to the prevention of endotoxemia in a murine model of inflammatory bowel disease', FASEB Journal, San Diego, California (2012) [E3]
Co-authors Philip Hansbro
2011 Kominsky D, Keely S, Macmanus C, Glover L, Scully M, Collins C, et al., 'Cellular methylation plays an anti-inflammatory role in Mucosal Inflammation', Inflammatory Bowel Diseases, Hollywood, Florida (2011) [E3]
2011 Keely S, Baird A, Kominsky D, Campbell E, Burgess A, Colgan S, 'HIF prolyl hydroxylase inhibition reverses disease symptoms in established TNBS colitis', Inflammatory Bowel Diseases, Hollywood, Florida (2011) [E3]
2011 Campbell E, Macmanus C, Kominsky D, Keely S, Glover L, Bowers B, et al., 'Resolvin E1-induced intestinal alkaline phosphatase promotes resolution of inflammation through LPS detoxification', Inflammatory Bowel Diseases, Hollywood, Florida (2011) [E3]
2011 Kominsky D, Keely S, Campbell E, Christopher M, Scully M, Collins C, et al., 'A central role of methylation in mucosal inflammation', Inflammatory Bowel Diseases, Hollywood, Florida (2011) [E3]
Show 46 more conferences
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Grants and Funding

Summary

Number of grants 46
Total funding $10,821,478

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


20214 grants / $2,375,332

Wheat proteins, the duodenal microbiome and immune activation in the aetiopathogenesis of non-coeliac gluten sensitivity and functional dyspepsia$2,025,110

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Simon Keely, Doctor Kerith Duncanson, Doctor Michael Potter, Mrs Natasha Koloski, Dr Emily Hoedt, Doctor Emily Hoedt, Miss Cheenie Nieva
Scheme Ideas Grants
Role Lead
Funding Start 2021
Funding Finish 2023
GNo G2000682
Type Of Funding C1100 - Aust Competitive - NHMRC
Category 1100
UON Y

In vivo assessment of proprietary drug candidates$169,701

Funding body: Microba Pty Limited

Funding body Microba Pty Limited
Project Team Professor Simon Keely
Scheme Research Grant
Role Lead
Funding Start 2021
Funding Finish 2021
GNo G2100429
Type Of Funding C3111 - Aust For profit
Category 3111
UON Y

Peri-operative factors affecting Natural Killer Cell function and their role in colorectal cancer re-occurrence and metastasis$120,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Simon Keely, Doctor Steve Smith, Joanne Soh
Scheme Research Grant
Role Lead
Funding Start 2021
Funding Finish 2024
GNo G2001397
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

2021 HMRI MRSP - Gastrointestinal Research $60,521

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Laureate Professor Nick Talley, Professor Simon Keely
Scheme NSW MRSP Infrastructure Grant
Role Investigator
Funding Start 2021
Funding Finish 2021
GNo G2100513
Type Of Funding C2220 - Aust StateTerritoryLocal - Other
Category 2220
UON Y

20204 grants / $422,026

In vitro and in vivo analysis of bile acid sequestrants. $264,700

Funding body: Viscera Labs, Inc

Funding body Viscera Labs, Inc
Project Team Professor Simon Keely, Laureate Professor Nick Talley, Doctor Bridie Goggins
Scheme Research Grant
Role Lead
Funding Start 2020
Funding Finish 2020
GNo G2000331
Type Of Funding C3211 - International For profit
Category 3211
UON Y

Animal model activity assessment of proprietary drug candidates$93,576

Funding body: Microba Pty Limited

Funding body Microba Pty Limited
Project Team Professor Simon Keely
Scheme Research Grant
Role Lead
Funding Start 2020
Funding Finish 2020
GNo G2001066
Type Of Funding C3111 - Aust For profit
Category 3111
UON Y

Identifying the food trigger for children with Eosinophilic Oesophagitis$40,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Adam Collison, Professor Joerg Mattes, Doctor Scott Nightingale, Professor Simon Keely
Scheme Research Grant
Role Investigator
Funding Start 2020
Funding Finish 2020
GNo G2000205
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Gut-Brain interactions in the development of Necrotising Enterocolitis$23,750

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Bridie Goggins, Doctor Julia Shaw, Professor Simon Keely, Doctor Aniruddh Deshpande, Doctor Peter Pockney
Scheme Project Grant
Role Investigator
Funding Start 2020
Funding Finish 2020
GNo G2000806
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

20196 grants / $2,895,388

Centre for Research Excellence in Digestive Health$2,543,731

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Nick Talley, Professor Sally Chan, Professor Simon Keely, Professor Marjorie Walker, Professor Gerald Holtmann, Associate Professor Michael Jones, Professor Mark Morrison, Professor Mark Morrison, Professor Sally Chan, Professor Jan Tack, Professor Peter Gibson, Professor Peter Gibson, Prof Jeff Coombes, Doctor Grace Burns
Scheme Centres of Research Excellence - Centres of Clinical Research Excellence (CRE)
Role Investigator
Funding Start 2019
Funding Finish 2024
GNo G1801219
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

In vivo and in vitro study of HIF stabilization through prolyla hydroxylase inhibition$146,597

Funding body: Gossamer Bio Inc

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

Rationale for the development of the Gastrointestinal Reprogramming Product (GaRP) Dietary Supplement$77,138

Funding body: Anatara Lifesciences Limited

Funding body Anatara Lifesciences Limited
Project Team Professor Simon Keely
Scheme Research Grant
Role Lead
Funding Start 2019
Funding Finish 2019
GNo G1900385
Type Of Funding C3111 - Aust For profit
Category 3111
UON Y

A Double-Blind Randomised Placebo-Controlled Trial Assessing the Effect of Peri-Operative Intravenous Lignocaine and Post-Operative Lignocaine Neurovascular Plane Infusion on Natural Killer Ce$60,000

Funding body: Colorectal Surgical Society of Australia and New Zealand Foundation Pty Ltd

Funding body Colorectal Surgical Society of Australia and New Zealand Foundation Pty Ltd
Project Team Doctor Steve Smith, Professor Simon Keely, Conjoint Professor Jonathan Gani, Doctor Gang Liu, Doctor Peter Pockney
Scheme Research Grant
Role Investigator
Funding Start 2019
Funding Finish 2019
GNo G1901026
Type Of Funding C3112 - Aust Not for profit
Category 3112
UON Y

The Applied Biosystems QuantStudio 6 Flex Real-Time PCR System$53,672

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Associate Professor Kirsty Pringle, Professor Simon Keely, Doctor Hannah Palliser, Doctor Jonathan Paul, Doctor Marina Ilicic, Doctor Lucy Murtha
Scheme Equipment Grant
Role Investigator
Funding Start 2019
Funding Finish 2019
GNo G1900306
Type Of Funding Scheme excluded from IGS
Category EXCL
UON Y

The Microbiome of Surgical Site Infections$14,250

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Simon Keely, Doctor Steve Smith, Doctor Peter Pockney
Scheme Project Grant
Role Lead
Funding Start 2019
Funding Finish 2019
GNo G1901238
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

20185 grants / $813,048

Hunter Cancer Biobank$538,523

Funding body: NSW Health Pathology - Pathology North

Funding body NSW Health Pathology - Pathology North
Project Team Professor Marjorie Walker, Laureate Professor Rodney Scott, Conjoint Professor Stephen Ackland, Mrs Susan Goode, Professor Pradeep Tanwar, Associate Professor Nikki Verrills, Professor Hubert Hondermarck, Doctor Simon King, Mr Ricardo Vilain, Associate Professor Nikola Bowden, Associate Professor Kelly Kiejda, Professor Simon Keely, Doctor Christopher Rowe
Scheme Research Grant
Role Investigator
Funding Start 2018
Funding Finish 2020
GNo G1800704
Type Of Funding C2220 - Aust StateTerritoryLocal - Other
Category 2220
UON Y

The role of microbial oxygen sensing in the development of anastomotic leaks$121,525

Funding body: Fisher & Paykel Healthcare Limited

Funding body Fisher & Paykel Healthcare Limited
Project Team Professor Simon Keely, Doctor Peter Pockney, Doctor Steve Smith
Scheme Research Consultancy
Role Lead
Funding Start 2018
Funding Finish 2019
GNo G1701624
Type Of Funding C3211 - International For profit
Category 3211
UON Y

Mary Sawyer Postgraduate Scholarship in Cancer Research$99,750

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Dr Georgia Carroll, Professor Simon Keely, Doctor Peter Pockney, Professor Marjorie Walker, Doctor Steve Smith, Doctor Andrea Johns
Scheme Postgraduate Research Scholarship
Role Lead
Funding Start 2018
Funding Finish 2021
GNo G1800612
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Non- immunosuppressive strategies for the treatment of IBD$33,250

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Simon Keely, Doctor Andrea Johns, Doctor Gang Liu
Scheme Project Grant
Role Lead
Funding Start 2018
Funding Finish 2018
GNo G1800196
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Analysis of luminal bacteria at the site of colorectal anastomoses and their association with anastomotic leaks$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Simon Keely, Doctor Peter Pockney, Doctor Steve Smith, Associate Professor Ian Grainge, Doctor Andrea Johns
Scheme Project Grant
Role Lead
Funding Start 2018
Funding Finish 2018
GNo G1701630
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

20174 grants / $2,018,737

Epithelial metabolism as a mediator of host-microbiome interactions in inflammatory bowel disease$857,419

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Simon Keely, Professor Mark Morrison, Dr Paraic O Cuiv, Associate Professor Martin Veysey, Associate Professor Susan Hua
Scheme Project Grant
Role Lead
Funding Start 2017
Funding Finish 2019
GNo G1600412
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

Investigating the role of hypoxia in tumour biology and microbiota interactions using a novel orthotopic model of colorectal cancer$587,136

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Professor Simon Keely
Scheme Career Development Fellowship
Role Lead
Funding Start 2017
Funding Finish 2019
GNo G1600818
Type Of Funding C2210 - Aust StateTerritoryLocal - Own Purpose
Category 2210
UON Y

Beyond the Next Generation of DNA Sequencing: Long Read Sequencing using Sequel$570,000

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Laureate Professor Rodney Scott, Professor Hubert Hondermarck, Associate Professor Kevin Spring, Doctor Anoop Enjeti, Mr Ricardo Vilain, Professor Christopher Scarlett, Associate Professor Kelly Kiejda, Doctor Heather Lee, Professor Simon Keely, Associate Professor Lei Jin
Scheme Research Equipment Grant
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1700427
Type Of Funding C2210 - Aust StateTerritoryLocal - Own Purpose
Category 2210
UON Y

Tramadol everted gut sac assay experiment$4,182

Funding body: Syntrix Biosystems

Funding body Syntrix Biosystems
Project Team Professor Simon Keely
Scheme Research Project
Role Lead
Funding Start 2017
Funding Finish 2017
GNo G1701010
Type Of Funding C3211 - International For profit
Category 3211
UON Y

20162 grants / $227,477

Biomarkers for functional gut disorders Australia (BFGD Australia)$207,477

Funding body: Commonwealth Diagnostics International Inc

Funding body Commonwealth Diagnostics International Inc
Project Team Laureate Professor Nick Talley, Professor Marjorie Walker, Professor Gerald Holtmann, Associate Professor Michael Jones, Professor Simon Keely
Scheme Commonwealth Laboratories Study
Role Investigator
Funding Start 2016
Funding Finish 2017
GNo G1601324
Type Of Funding C3211 - International For profit
Category 3211
UON Y

Emlyn and Jennie Thomas Postgraduate Medical Research Scholarship$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Miss Bridie Goggins, Professor Simon Keely, Professor Darryl Knight, Associate Professor Jay Horvat
Scheme Postgraduate Research Scholarship
Role Lead
Funding Start 2016
Funding Finish 2017
GNo G1600721
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

20154 grants / $514,201

Chlamydia and reproductive health $475,526

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team

Kenneth Beagley

Scheme Project Grant
Role Investigator
Funding Start 2015
Funding Finish 2018
GNo
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON N

A novel model of colorectal cancer for studying personalised tumour biology, metastasis and the role of the microbiome$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Simon Keely
Scheme Project Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1501436
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Too Much of a Good Thing: Application for a triple-gas incubator to allow cell culture under normal conditions$16,675

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Craig Gedye, Laureate Professor Rodney Scott, Associate Professor Nikola Bowden, Professor Simon Keely, Associate Professor Kathryn Skelding
Scheme Research Grant
Role Investigator
Funding Start 2015
Funding Finish 2015
GNo G1500730
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Experimental Biology 2015, Boston USA, 26 March-1 April 2015$2,000

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

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Professor Simon Keely
Scheme Travel Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1500204
Type Of Funding Internal
Category INTE
UON Y

20146 grants / $647,043

Spinal processing of sensory signals from the gut$554,477

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Conjoint Professor Robert Callister, Professor Simon Keely, Associate Professor Brett Graham, Professor Alan Brichta, Dr David Hughes
Scheme Project Grant
Role Investigator
Funding Start 2014
Funding Finish 2017
GNo G1300361
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

Activating natural protective and healing responses in chronic inflammatory bowel disease$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Simon Keely, Doctor Ellen Marks, Associate Professor Martin Veysey
Scheme Research Grant
Role Lead
Funding Start 2014
Funding Finish 2014
GNo G1401453
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

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, Professor Jodie Simpson, Professor Lisa Wood, Professor Liz Milward, Dr NATHAN Bartlett, Professor 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

Hypoxia Chamber –Glovebox$22,000

Funding body: Faculty of Health, University of Newcastle

Funding body Faculty of Health, University of Newcastle
Scheme Equipment GRant
Role Lead
Funding Start 2014
Funding Finish 2015
GNo
Type Of Funding Internal
Category INTE
UON N

The role of the microbiome in the development of food allergy$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Simon Keely, Associate Professor Jay Horvat
Scheme Project Grant
Role Lead
Funding Start 2014
Funding Finish 2014
GNo G1301344
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Experimental Biology 2014, San Diego USA, 26-30 April 2014$2,000

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

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Professor Simon Keely
Scheme Travel Grant
Role Lead
Funding Start 2014
Funding Finish 2014
GNo G1400253
Type Of Funding Internal
Category INTE
UON Y

20132 grants / $22,000

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, Professor Jodie Simpson, Professor Rakesh Kumar, Doctor Nicole Hansbro, Doctor Steven Maltby, Doctor Ming Yang, Doctor Gerard Kaiko, Associate Professor Jay Horvat, Professor 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

United European Gastroenterology Week, Berlin, 12 -16 October 2013$2,000

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

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Professor Simon Keely
Scheme Travel Grant
Role Lead
Funding Start 2013
Funding Finish 2014
GNo G1300842
Type Of Funding Internal
Category INTE
UON Y

20124 grants / $444,226

The Role of Hypoxia in Wound Healing During Mucosal Inflammation$312,726

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Simon Keely
Scheme Project Grant
Role Lead
Funding Start 2012
Funding Finish 2014
GNo G1100095
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

Karl Storz, Small animal endoscopy suite$80,000

Funding body: Faculty of Health, University of Newcastle

Funding body Faculty of Health, University of Newcastle
Scheme Faculty of Health, Equipment Grant
Role Lead
Funding Start 2012
Funding Finish 2015
GNo
Type Of Funding Internal
Category INTE
UON N

SpectraMax M5e Multi-Mode Microplate Reader$50,000

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Professor Phil Hansbro, Professor Joerg Mattes, Professor Rakesh Kumar, Doctor Nicole Hansbro, Doctor Ming Yang, Associate Professor Jay Horvat, Professor Simon Keely, Doctor Andrew Jarnicki, Doctor Linda Howland, Doctor Kelly Asquith
Scheme Equipment Grant
Role Investigator
Funding Start 2012
Funding Finish 2012
GNo G1100975
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

Experimental Biology 2012, San Diego, USA, 21 - 25 April 2012$1,500

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

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Professor Simon Keely
Scheme Travel Grant
Role Lead
Funding Start 2012
Funding Finish 2013
GNo G1200426
Type Of Funding Internal
Category INTE
UON Y

20112 grants / $46,500

SCIREQ FlexiVentFX system + FlexiVentFX extension$45,000

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 Joerg Mattes, Professor Simon Keely, Associate Professor Jay Horvat, Doctor Nicole Hansbro, Doctor Ming Yang, Doctor Catherine Ptaschinski, Doctor Kelly Asquith, Doctor Gough Au, Conjoint Professor Peter Wark, Laureate Professor John Aitken, Conjoint Professor Keith Jones, Laureate Professor Roger Smith, Professor Judith Black, Professor Rakesh Kumar, Professor Paul Hertzog
Scheme Equipment Grant
Role Investigator
Funding Start 2011
Funding Finish 2011
GNo G1100037
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

Gastrointestinal Tract: XIV: Stems Cells, Adaptation, Inflammation and Cancer, Steamboat Sprngs, Colorado, USA, 14 - 18 August 2011$1,500

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

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Professor Simon Keely
Scheme Travel Grant
Role Lead
Funding Start 2011
Funding Finish 2012
GNo G1100679
Type Of Funding Internal
Category INTE
UON Y

20092 grants / $335,500

Influence of Hypoxia and HIF Activation on Intestinal Epithelial Restitution via Integrin Signaling$175,500

Funding body: Crohn's and Colitis Foundation of America

Funding body Crohn's and Colitis Foundation of America
Project Team

Simon Keely

Scheme Research Fellowship
Role Lead
Funding Start 2009
Funding Finish 2011
GNo
Type Of Funding International - Competitive
Category 3IFA
UON N

Microbiome adaption during intestinal fluid transport$160,000

Funding body: Takeda Pharmaceuticals North America, Inc

Funding body Takeda Pharmaceuticals North America, Inc
Project Team

Sean Colgan

Scheme Investigator Initiated - Sponsored Research
Role Investigator
Funding Start 2009
Funding Finish 2011
GNo
Type Of Funding Not Known
Category UNKN
UON N

20071 grants / $60,000

Influence of intestinal fluid transport on bacterial invasion.$60,000

Funding body: Takeda Pharmaceuticals North America, Inc

Funding body Takeda Pharmaceuticals North America, Inc
Project Team

Sean Colgan

Scheme Investigator Initiated - Sponsored Research
Role Investigator
Funding Start 2007
Funding Finish 2008
GNo
Type Of Funding International - Competitive
Category 3IFA
UON N
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Research Supervision

Number of supervisions

Completed9
Current16

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2021 PhD Immune Screening as a Predictor of Food Triggers for Relapse in Crohn’s Disease. PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle Principal Supervisor
2021 PhD Peri-Operative Factors Affecting Natural Killer Cell Function and Their Role in Colorectal Cancer Re-Occurrence and Metastasis PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle Principal Supervisor
2021 PhD The Role of Microbial Oxygen Sensing in the Development of Anastomotic Leaks PhD (Surgical Science), College of Health, Medicine and Wellbeing, The University of Newcastle Principal Supervisor
2020 PhD Epigenetic Heterogeneity and Dynamics in Acute Myeloid Leukaemia PhD (Medical Genetics), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2020 PhD Investigating the Pathophysiology and Treatment of Rumination Syndrome PhD (Medicine), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2020 PhD Microbiome and Immune-Phenotyping of Dietary Wheat Sensitivity PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle Principal Supervisor
2020 PhD Diverticular Disease and Diverticular Inflammation Histological Subsets and the Influence of the Microbiome on Disease Outcomes PhD (Anatomical Pathology), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2019 PhD The Eosinophilc Microbiota - The Influence of Eosinophilia on the Mucosal Hostmicrobiota Homeostasis PhD (Paediatric & Child Hlth), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2019 PhD Interactions between Taste, Diet and the GI Microbiota; Consequences for Metabolic Health. PhD (Food Science), College of Engineering, Science and Environment, The University of Newcastle Co-Supervisor
2018 PhD The Impact of Perinatal Immune Challenge and Adolescent Stress on Gastrointesinal Inflammation and Integrity and the Relationship with Anxiety PhD (Psychology - Science), College of Engineering, Science and Environment, The University of Newcastle Co-Supervisor
2018 PhD Mechanisms of nocturnal airway hyperresponsiveness in asthma PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2018 PhD Microbiome of Surgical Site PhD (Anatomy), College of Health, Medicine and Wellbeing, The University of Newcastle Principal Supervisor
2017 PhD The Role of Dietary Wheat in Functional Dyspepsia: Defining an Overlap with Gluten or Wheat Sensitivity PhD (Medicine), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2017 PhD The Impact of Surgery, Inflammation and Sepsis on Neutrophil Extracellular Trap (NET) Formation and Subsequent Metastatic Disease in Colorectal Cancer PhD (Surgical Science), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2017 PhD Modulation of the Microbiota in Irritable Bowel Syndrome PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle Principal Supervisor
2017 PhD Mechanisms of Stress-Induced Intestinal Inflammation in GI 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 Characterising the Immunopathology of Functional Dyspepsia PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle Principal Supervisor
2020 PhD Characterising how Chronic Stress and Natural Rewards Impact Lateral Hypothalamic Circuitry PhD (Anatomy), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2019 PhD In Vitro And in Vivo Investigations of the a-Integrins Regulated by Hypoxia Inducible Factor (HIF)-1 Signalling during Mucosal Wound Healing PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle Principal Supervisor
2018 PhD Investigation of the Pathogenesis of Influenza Infection in Asthma and COPD; Potential Therapeutic Interventions PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2017 PhD Investigation of Visceral Sensory Processing Mechanisms in the Superficial Dorsal Horn of the Spinal Cord PhD (Anatomy), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2017 PhD Mechanisms of Predisposition to Secondary Bacterial Pneumonia PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2017 PhD The Role of Mast Cell Proteases in Respiratory Disease PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2017 PhD Mechanisms of Lung Inflammation Associated with Inflammatory Bowel Disease PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle Principal Supervisor
2016 PhD Investigation of Pathogenesis of Chronic Obstructive Pulmonary Disease PhD (Immunology & Microbiol), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
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Research Collaborations

The map is a representation of a researchers co-authorship with collaborators across the globe. The map displays the number of publications against a country, where there is at least one co-author based in that country. Data is sourced from the University of Newcastle research publication management system (NURO) and may not fully represent the authors complete body of work.

Country Count of Publications
Australia 109
United States 23
United Kingdom 20
Ireland 16
Canada 3
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News

Great ideas attract $7 million in NHMRC grants

December 18, 2020

Seven University of Newcastle researchers have been awarded more than $7 million in National Health and Medical Research Council (NHMRC) Ideas Grants, designed to support innovative and creative research projects which address a specific question.

Professor Simon Keely

Position

Professor
Gastrointestinal Research Group
School of Biomedical Sciences and Pharmacy
College of Health, Medicine and Wellbeing

Focus area

Immunology and Microbiology

Contact Details

Email simon.keely@newcastle.edu.au
Phone (02) 4042 0229 (HMRI)
Fax (02) 4042 0026 (HMRI)

Office

Room Rm 3409 Lvl 3 East Wing (HMRI)
Building HMRI
Location HMRI

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