IDDF2021-ABS-0200 Bacillus amyloliquefaciens combined with resistant starch to ameliorate intestinal inflammation

作者
Hailan Zhao,Yao Peng,Jing Xu,Haoming Xu,Wenqi Huang,Jiaqi Wang,Xue Guo,Yong Zhang,Hongli Huang,Youlian Zhou,Yuqiang Nie
标识
DOI:10.1136/gutjnl-2021-iddf.58
摘要

Background Bacillus amyloliquefaciens (BA) decomposes starch by producing alpha-amylase to produce short-chain fatty acids (SCFA). Resistant starch (RS) can be fermented by colonic microbiota and metabolized to SCFA containing acetic acid and butyric acid by which can ameliorate intestinal inflammation. In this study, dextran sulfate sodium (DSS)-induced colitis mouse model was administrated to assess the therapeutic effect of BA combined with RS in experimental colitis. Methods 6-week-old male BALB/c mice were given 3% DSS drinking water for 1 week to induce acute colitis. Mice were fed with maintenance forage as control group. The content of RS was 465.692g/kg, and the abundance of BA by gavage administration in mice was 1*107 CFU for 7 days. The mice were administered daily, including weight loss and disease activity index (DAI). The mice were sacrificed on the eighth day. We collect specimens, measure colon length, evaluate histopathologic score and detect the level of IL-1β, IL-6, TNF-αand occludin of intestinal tissue by qPCR. Results Weight loss and DAI were more effectively improved in the live BA combined with RS than administered RS alone. Colonic inflammation was significantly alleviated in the live BA combined with RS. The colon length and histopathologic score of live BA combined with RS intervention were more improved than that of the control (p<0.001), including a smaller extent of intestinal epithelial damage and crypt structure disorder. The degree of inflammatory cell infiltration was lighter (p=0.029). The expression of IL-1β (p=0.008), IL-6 (p=0.02) and TNF-α (p<0.001) were reduced and the expression of Occludin (p =0.006) was increased than RS alone. Conclusions The intervention of BA combined with RS may ameliorate DSS-induced acute colitis and promote colon barrier recovery.

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