Chlamydia Muridarum Antagonized DSS-induced Colitis In Mice By Mediating IL-22 And Occludin

Objective: Ulcerative colitis(UC)is the most common inflammatory bowel disease,and its incidence has increased in recent years.Recent clinical and experimental data indicate that gut microbiota plays a pivotal role in the pathogenesis of UC.Chlamydia establishes a stable and persistent colonization in the gastrointestinal tract without apparent pathogenicity to gastrointestinal or extra-gastrointestinal tissues.However,the detailed effects of Chlamydia on the gastrointestinal tissue remain unknown.In this project,an experimental colitis model induced by dextran sodium sulfate(DSS)was established to study the effect of Chlamydia muridarum(C.muridarum)infection on the levels of IL-22 and occludin in the colon tissue of colitis mice,and to explore and analyze the effect of chlamydia on DSS-induced colitis and its mechanism,and provide a new target for the clinical treatment of colitis and strategy.Methods: The infection model of C.muridarum mice was established by gavage on C57BL/6J mice.After 28 days of successful modeling,dextran sodium sulfate(DSS)was induced to establish experimental colitis model.The experiment was divided into three groups:Control group,model group(DSS group),and intervention group(CM+DSS group).The changes of body weight,disease activity index(DAI),colon length and related pathological changes of mice in each group were detected.Protein expression levels of IL-22 and occludin in colonic tissues of mice in each group were determined by western blot.The mice were divided into Control group,DSS group,CM+DSS group,and CM+DSS+IL-22 antagonist group.Changes in body weight,DAI,colon length were detected in various mice.The protein expressions of IL-22 and occludin in colon tissues of mice in each group were determined by western blot.Results: C.muridarum improved significantly colitis symptoms including body weight loss,disease activity index,colon length change(P<0.05)and histopathological change of colon caused by DSS,and reversed the expression of Interleukin-22(IL-22)and occludin(P<0.05)in colon tissue that decreased following DSS administration.Furthermore,the absence of IL-22 completely prevented C.muridarum from alleviating colitis and made occludin,an important downstream effector protein of IL-22,to decrease significantly(P<0.05).Conclusion: Based on the successful use of DSS to construct an experimental colitis model,we found that C.muridarum antagonized DSS-induced colitis in mice by mediating the IL-22 and occludin.