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) Ⅳinduced 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 .