Intestinal mucosal barriers help the body resist many intestinal inflammatory diseases, such as inflammatory bowel disease (IBD). In this study, we identified a novel bacterium promoting the repair of intestinal mucosa and investigated the potential mechanisms underlying its activity. Culture supernatant of Bacillus subtilis RZ001 upregulated the expression of mucin 2 (MUC2) and tight junction (TJ) proteins in HT-29 cells in vitro. Oral administration of B. subtilis RZ001 may have significantly reduced symptoms such as the dextran sulfate sodium (DSS)-induced decrease in body weight, shortening of colon length and overproduction of proinflammatory factors. The number of goblet cells and levels of MUC2 and TJ proteins were significantly increased in adult mice fed with B. subtilis RZ001. B. subtilis RZ001 cells upregulated the levels of MUC2 in the intestinal organoids. Furthermore, culture supernatant of B. subtilis RZ001 could suppress the Notch signalling pathway and activate the expression of atonal homolog 1 (Atoh1). The transcription factor Atoh1 is required for intestinal secretory cell differentiation and activates transcription of MUC2 via binding to E-boxes on the MUC2 promoter. Taken together, B. subtilis strain RZ001 has the potential for treating IBD. The present study is helpful to elucidate the mechanisms of B. subtilis action.

中文翻译：

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枯草芽孢杆菌RZ001通过抑制Notch信号通路和激活ATOH-1来改善肠道完整性并减轻结肠炎。

肠粘膜屏障可帮助人体抵抗多种肠道炎症，例如炎症性肠病（IBD）。在这项研究中，我们确定了一种新型细菌，可促进肠道粘膜的修复，并研究了其活性的潜在机制。枯草芽孢杆菌RZ001的培养上清液在体外可上调HT-29细胞中粘蛋白2（MUC2）和紧密连接（TJ）蛋白的表达。口服枯草芽孢杆菌RZ001可能具有明显减轻的症状，例如右旋糖酐硫酸钠（DSS）引起的体重下降，结肠长度缩短和促炎因子的过度产生。在用枯草芽孢杆菌RZ001喂养的成年小鼠中，杯状细胞的数量以及MUC2和TJ蛋白的水平显着增加。枯草芽孢杆菌RZ001细胞上调了肠道类器官中MUC2的水平。此外，枯草芽孢杆菌RZ001的培养上清液可以抑制Notch信号通路并激活非同源同源物1（Atoh1）的表达。肠道分泌细胞分化需要转录因子Atoh1，并通过与MUC2启动子上的E-box结合来激活MUC2的转录。在一起枯草芽孢杆菌菌株RZ001具有治疗IBD的潜力。本研究有助于阐明枯草芽孢杆菌的作用机制。