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Schistosoma japonicum ova maintains epithelial barrier function during experimental colitis

Author(s): Chen-Mei Xia | Yuan Zhao | Li Jiang | Jie Jiang | Shun-Cai Zhang

Journal: World Journal of Gastroenterology
ISSN 1007-9327

Volume: 17;
Issue: 43;
Start page: 4810;
Date: 2011;
Original page

Keywords: Crohn’s disease | Schistosoma japonicum ova | Tight junction protein | ZO-1 | Occludin

AIM: To evaluate the impacts of Schistosoma japonicum (S. japonicum) ova on the tight junction barriers in a trinitrobenzenesulfonic acid (TNBS)-induced colitis model. METHODS: Balb/c mice were randomly divided into three groups: control group; TNBS+ova- group and TNBS+ova+ group. TNBS was used intracolonic to induce colitis and mice of the TNBS+ova+ group were pre-exposed to S. japonicum ova as a prophylactic intervention. Colon inflammation was quantified using following variables: mouse mortality, weight loss, colon extent and microscopic inflammation score. Serum expression of tumor necrosis factor-α and interferon-γ were assessed to evaluate the systemic inflammatory response. NOD2 and its mRNA were also tested. Bacterial translocations were tested by culturing blood and several tissues. ZO-1 and occludin were chosen as the representations of tight junction proteins. Both the proteins and mRNA were assessed. RESULTS: Ova pre-treatment contributed to the relief of colitis and decreased the mortality of the models. NOD2 expression was significantly downregulated when pretreated with the ova. The TNBS injection caused a significant downregulation of ZO-1 and occludin mRNA together with their proteins in the colon; ova pre-exposure reversed these alterations. Treatment with S. japonicum ova in the colitis model caused lower intestinal bacterial translocation frequency. CONCLUSION: S. japonicum ova can maintain epithelial barrier function through increasing tight junction proteins, thus causing less exposure of NOD2 to the luminal antigens which may activate a series of inflammatory factors and induce colitis.

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