Abstract
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 extragastrointestinal tissues. However, the detailed effects of Chlamydia on the gastrointestinal tissue remain unknown. The primary aim of this study is to investigate the effects of Chlamydia muridarum (C. muridarum) on development of colitis induced by dextran sodium sulfate (DSS) and the underlying molecular mechanism. The results suggested that C. muridarum significantly improved colitis symptoms—including weight loss, disease activity index, colon length, and histopathological changes in the colon caused by DSS—and alleviated the reduced expression of interleukin-22 and occludin in the colonic tissue due to DSS administration. Furthermore, the absence of IL-22 completely prevented C. muridarum from alleviating colitis and significantly decreased the levels of occludin, an important downstream effector protein of IL-22. These findings suggest that C. muridarum ameliorates ulcerative colitis induced by DSS via the IL-22/occludin signal pathway.
Highlights
Ulcerative colitis (UC), a type of inflammatory bowel disease, is a chronic and relapsing inflammatory disorder of the gastrointestinal (GI) tract with a rapidly increasing incidence worldwide [1]
To determine whether C. muridarum can colonize the gastrointestinal tract of female mice stably and for long periods, we monitored the growth of C. muridarum in the GI tract of intragastrically inoculated mice using immunofluorescence assays (Table 1)
Chlamydial organisms have been detected in the GI tracts of both humans and animals and C. muridarum is known to colonize the GI tract for long periods, the medical significance of these phenomena remains unclear [19]
Summary
Ulcerative colitis (UC), a type of inflammatory bowel disease, is a chronic and relapsing inflammatory disorder of the gastrointestinal (GI) tract with a rapidly increasing incidence worldwide [1]. The gut microbiota regulates immune pathways, which is demonstrated by IL-22 response and barrier maintenance by epithelial tight junctions, and plays a key role in triggering UC [3]. IL-22, an important factor in the pathogenesis of UC as demonstrated by experiment models of colitis [5], induces the expression of tight-junction proteins (e.g., occludin and ZO-1) to facilitate gut epithelial resistance to colitis, indicating that IL-22 protects the intestinal mucosa from inflammation by upregulating the production of tightjunction proteins [6]. Impaired occludin, which disrupts the epithelial barrier integrity, was observed in both human UC and mouse model of colitis induced by dextran sodium sulfate (DSS) [8]. IL-22/occludin signal pathway is important in colitis
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