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微小克里斯滕森菌通过调节炎症来保护和修复结肠炎模型中的肠道屏障。

Christensenella minuta protects and restores intestinal barrier in a colitis mouse model by regulating inflammation.

机构信息

Micalis Institute, AgroParisTech, INRAE, Université Paris-Saclay, 68350, Jouy-en-Josas, France.

YSOPIA Bioscience, 33076, Bordeaux, France.

出版信息

NPJ Biofilms Microbiomes. 2024 Sep 19;10(1):88. doi: 10.1038/s41522-024-00540-6.

Abstract

Christensenella minuta DSM 22607 has recently been suggested as a potential microbiome-based therapy for inflammatory bowel disease (IBD) because it displays strong anti-inflammatory effects both in vitro and in vivo. Here, we aimed to decipher the mechanism(s) underlying the DSM 22607-mediated beneficial effects on the host in a mouse model of chemically induced acute colitis. We observed that C. minuta plays a key role in the preservation of the epithelial barrier and the management of DNBS-induced inflammation by inhibiting interleukin (IL)-33 and Tumor necrosis factor receptor superfamily member 8 (Tnfrsf8) gene expression. We also showed that DSM 22607 abundance was positively correlated with Akkermansia sp. and Dubosiella sp. and modulated microbial metabolites in the cecum. These results offer new insights into the biological and molecular mechanisms underlying the beneficial effects of C. minuta DSM 22607 by protecting the intestinal barrier integrity and regulating inflammation.

摘要

Christensenella minuta DSM 22607 最近被提议作为一种基于微生物组的治疗炎症性肠病(IBD)的方法,因为它在体外和体内均显示出强烈的抗炎作用。在这里,我们旨在在化学诱导的急性结肠炎小鼠模型中破译 DSM 22607 对宿主产生有益影响的潜在机制。我们观察到 C. minuta 通过抑制白细胞介素 (IL)-33 和肿瘤坏死因子受体超家族成员 8 (Tnfrsf8) 基因表达,在保护上皮屏障和管理 DNBS 诱导的炎症方面发挥关键作用。我们还表明,DSM 22607 的丰度与 Akkermansia sp. 和 Dubosiella sp. 呈正相关,并调节盲肠中的微生物代谢物。这些结果为 C. minuta DSM 22607 通过保护肠道屏障完整性和调节炎症产生有益影响的生物学和分子机制提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8953/11411060/15d570d52aa5/41522_2024_540_Fig1_HTML.jpg

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