Flightless I exacerbation of inflammatory responses contributes to increased colonic damage in a mouse model of dextran sulphate sodium-induced ulcerative colitis.

ABSTRACT: Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by cytokine driven inflammation that disrupts the mucosa and impedes intestinal structure and functions. Flightless I (Flii) is an immuno-modulatory protein is a member of the gelsolin family of actin-remodelling proteins that regulates cellular and inflammatory processes critical in tissue repair. Here we investigated its involvement in UC and show that Flii is significantly elevated in colonic tissues of patients with inflammatory bowel disease. Using an acute murine model of colitis, we characterised the contribution of Flii to UC using mice with low (Flii^+/-), normal (Flii^+/+) and high Flii (Flii^Tg/Tg). High levels of Flii resulted in significantly elevated disease severity in

SUBMITTER: Kopecki Z 

PROVIDER: S-EPMC6728368 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature