〔Abstract〕 Objective To investigate the role of mast cell(MC) in the progression of inflammatory bowel disease(IBD) and the possible regulatory mechanisms. Methods Wild type mice, MC-deficient mice and MC reconstituted mice were used to construct dextran sodium sulfate(DSS)-induced colitis models. Assays such as toluidine blue staining, flow cytometry and Real-time quantitative PCR were used to analyze results. Results MCs migrated and infiltrated to the intestine under the induction of stem cell factor(Scf) and matrix metalloprotein 9(Mmp-9) factors. In the mouse IBD models, the integrity of intestinal mucosal villi in MC-deficient mice was worse than that in WT mice. In MC-deficient mice, the intestinal inflammation was more severe and the ability of mucosal repair was worse. After MC reconstruction, intestinal inflammation was reduced and mucosal repair ability was restored. The ratio of macrophage M1/M2 in WT mouse was lower than that in MC-deficient mouse. The genes interleukin-4(Il4) and interleukin-10(Il10) associated with M2 macrophages were higher in the WT mouse than in the MC-deficient mouse, and other anti-inflammatory factor genes interleukin-13(Il13) and GATA binding protein 3(Gata3) were also higher than those in the WT group. The pro-inflammatory factor gene inducible nitric oxide synthase(Inos) was opposite. Conclusion MC polarizes macrophages to exert anti-inflammatory and promote mucosal repair in the process of IBD.