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Faecalibacterium prausnitzii-derived microbial anti-inflammatory molecule regulates intestinal integrity in diabetes mellitus mice via modulating tight junction protein expression.
Journal of Diabetes ( IF 4.5 ) Pub Date : 2019-10-30 , DOI: 10.1111/1753-0407.12986
Jihao Xu 1 , Rongrong Liang 2 , Wang Zhang 1, 3 , Kuangyi Tian 1 , Jieyao Li 1 , Xianming Chen 4 , Tao Yu 1 , Qikui Chen 1
Affiliation  

Impaired intestinal barrier structure and function have been validated as an important pathogenic process in type 2 diabetes mellitus (T2DM). Gut dysbiosis is thought to be the critical factor in diabetic intestinal pathogenesis. As the most abundant commensal bacteria, Faecalibacterium prausnitzii (F. prausnitzii) play important roles in gut homeostasis. The microbial anti‐inflammatory molecule (MAM), an F. prausnitzii metabolite, has anti‐inflammatory potential in inflammatory bowel disease (IBD). Thus, we aimed to explore the function and mechanism of MAM on the diabetic intestinal epithelium.

中文翻译:

费氏杆状杆菌来源的微生物抗炎分子通过调节紧密连接蛋白的表达来调节糖尿病小鼠的肠道完整性。

肠道屏障结构和功能受损已被证实是2型糖尿病(T2DM)的重要致病过程。肠道营养不良被认为是糖尿病肠道发病机制的关键因素。作为最丰富的共生细菌,普氏不动杆菌(F.calius prausnitzii)在肠道稳态中起着重要的作用。微生物F.prausnitzii代谢产物抗炎分子(MAM)在炎症性肠病(IBD)中具有抗炎潜力。因此,我们旨在探讨MAM在糖尿病肠上皮细胞中的功能和机制。
更新日期:2019-10-30
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