The Eri Group - Cell Stress, Inflammation and Immunity

The hierarchical activation 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.