CD1d knockout mice can antagonize DSS-induced colitis

LI Jiao; CHEN Yongwen; ZHANG Qinggao

doi:10.13431/j.cnki.immunol.j.20180117

Abstract：This study designed to observe the effect of CD1d in the progress of mouse colitis by using the dextran sulfate sodium (DSS)-induced colitis model of CD1d-/-(genetic background: C57BL/6) mice. The colitis mouse model was established by immunization of CD1d-/-(genetic background: C57BL/6) mice and C57BL/6 mice.They were given daily 2.5％ DSS feeding for 6 days. The changes in body weight, fecal traits, activity conditions were recorded every day. Disease activity index (DAI) of mice was assessed and the survival of the mice was recorded.On the 6 thday, intestinal permeability was measured by FITC-dextran gavage and the length of the colon was measured. The histopathological changes of the colon were observed by HE staining. The intestinal epithelial proliferation was detected by immunohistochemistry and immunofluiorescence. Western blot was used to detect the expression of inflammatory cytokines in colon tissue of mice.Data showed that compared with the WT mice of, the survival of CD1d-/-mice was higher (P＜0.05), the weight loss was slower and disease activity index (DAI) was lower (P＜0.05), and the colon length was longer and intestinal permeability was lower (P＜0.01), intestinal mucosal damage was lighter and colonic epithelial positive cells proliferated significantly (P＜0.05). The expression levels of IL-1 beta and IL-18 were highter (P＜0.05).These combined data suggest that CD1d knockout mice can antagonize DSS-induced colitis may by promoting colon expression of NLRP3 inflammasome and its substrates IL-1 beta and IL-18.