P075 Evolutive profile of biomarkers in postoperative Crohn's disease patients: identification of recurrence risk predictors

Results: Chronic DSS colitis induced persistent thickening of the muscularis propria (MP) with infiltration of vimentin+ cells in the chronic phase but not in acute colitis. Moreover, a mucosal healing response was associated with more cycles and recovery. Myofibroblasts (vimentin+ a-SMA+) were present in the submucosa (SM) in the chronic phase and not in the acute model. Differential deposition of collagen I and III was observed: collagen I was present in the SM around vimentin+ cells. Collagen III deposition in the SM started in the acute phase, further increased in chronic colitis with infiltration of collagen III between smooth muscle cells of the MP, to intestinal stricture formation in CD. During prolonged recovery there was a decrease in collagen III. Tenascin expression was scant in control colon but was clearly present in the mucosa and SM in the acute phase in individual cells. A linear deposition of tenascin around the crypts was also seen as expected in acute colitis. The linear deposition in the mucosa and submucosal spots persisted after 2 cycles of DSS, correlating with persisting tissue damage. The expression of tenascin decreased after 3 cycles and more so after additional recovery, in association with the disappearance of tissue damage. Conclusions: The connective tissue changes observed in chronic murine colitis induced by repeated cycles of DSS reflects tissue remodeling as seen in CD. The technical ease and reproducibility of the DSS model and ability to induce it in mice of a common inbred strain makes it an attractive model to study the connective tissue changes occurring in IBD.