Cell Stress, Inflammation and Immunity
The major research aim of Cell Stress, Inflammation and Immunity research group is to identify the causes of chronic gut inflammation and colorectal cancer and identify strategies to prevent and treat these conditions. Our research group investigates conditions affecting gut health by through clinical research and clinical trials. Our work involves in-vitro cell line work, pre-clinical models of gut disease and colon cancer, research with human clinical samples and clinical trials in humans.
Research Interests and alignment
Our group's research interests include the role of inflammasomes on bowel diseases and bowel cancer, early stage carcinogenesis pathways in colorectal cancer and the role of cytokines in inflammatory bowel disease (IBD) pathogenesis, colorectal cancer pathways, heparin as anti-inflammatory agent in colitis, the role of bitter melon as anti-ER stress agent, and the epidemiology of IBD in Tasmania.
We have significant expertise in the fields of colitis and IBD, which includes a multitude of animal models of colitis. All the clinical, histological, immunological and immuno-histochemical methods have been optimised and are in current use in our research laboratory.
- Chronic Inflammation
- ER stress
- Pathogenesis of inflammatory Bowel Disease
- Gut Health
- Pre-clinical models of gut health
- The hierarchial activation of of inflammasomes in chronic colitis
Inflammasomes are protein complexes that are implicated in initiation of many diseases including inflammatory bowel disease (IBD). In our laboratory, we have characterised a mouse model that develops spontaneous colitis similar to human colitis. We have a strong indication from human studies that specific inflammasomes are activated in IBD. In this mouse model, we want to explore functional studies as to how inflammasome contributes to pathogenesis of IBD.
- Characterisation of flat dysplasia in colitis associated colorectal cancer
Patients with ulcerative colitis are at increased risk of developing colorectal cancer. Colitis-associated colorectal cancer (CACC) progresses through similar stepwise gene mutations observed in sporadic cancers, but the sequence in which they occur is reversed. Understanding the transition from colitis to tumour requires relevant animal models. Colonic carcinogenesis has been modelled using genotoxic carcinogens such as azoxymethane. We hypothesise that exacerbation of pre-existing chronic colitis in a Muc2 mutant (Winnie) mouse strain with dextran sulphate sodium (DSS) would induce colorectal tumorigenesis.
- CCR6 deficiency aggravates colitis in a spontaneous colitis model
Chemokine receptor 6 (CCR6) and its ligand CCL20 is implicated to play a major role in IBD pathogenesis. The CCR6/CCL20 axis is involved in both immune regulation and activation. CCR6 is expressed by both pro-inflammatory cells and regulatory T cells elucidate the dual role of the receptor. The contradictory role of CCR6/CCL20 in inflammation/homeostasis requires further research.
For more information about current projects please contact Dr Raj Eri email@example.com.
- Prof Heinrich Korner - MRIT and University of Tasmania
- Assoc Prof Nuri Guven - Division of Pharmacy, University of Tasmania
- Dr Rahul Patel - Division of Pharmacy, University of Tasmania
- Dr Lana Shabala - School of Land and Foo,d University of Tasmania
- Dr Roger Stanley - DSTO, Scottsdale & School of Land and Food, University of Tasmania
- Dr Kulmira Nurgali - Victoria University, Melbourne
- Drs Brent Mitchell, Scott Fanning, Ray Wilson - Launceston General Hospital, Tasmania
- Dr Prathiba Nerurkar - University of Hawaii, U.S.A.
- Dr Marcello Chieppa - Bari University, Italy
- Prof Mike McGuckin - Mater Medical Research Institute/TRI, University of Queensland, Brisbane
Our research group has attracted total of over $1 million in 15 research grants in the last 5 years from NHMRC, Cancer Council Tasmania, Clifford-Craig Medical Research Trust, Rotary Club, Industry Fund and multiple UTAS internal grants.
For further information on current and/or future projects, please contact Dr Raj Eri.