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普拉梭菌及其上清液可增加产生短链脂肪酸的细菌,以恢复三硝基苯磺酸诱导的结肠炎中的肠道菌群失调。

F. prausnitzii and its supernatant increase SCFAs-producing bacteria to restore gut dysbiosis in TNBS-induced colitis.

作者信息

Zhou Youlian, Xu Haoming, Xu Jing, Guo Xue, Zhao Hailan, Chen Ye, Zhou Yongjian, Nie Yuqiang

机构信息

Department of Gastroenterology, Guangzhou Digestive Disease Center, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, No. 1 Panfu Road, Guangzhou, 510180, China.

Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.

出版信息

AMB Express. 2021 Feb 28;11(1):33. doi: 10.1186/s13568-021-01197-6.

Abstract

An increasing number of studies have shown that Faecalibacterium prausnitzii (F. prausnitzii) is a promising anti-inflammatory bacterium that colonizes in the gut and that gut microbiota dysbiosis plays an important role in the pathogenesis of inflammatory bowel disease (IBD). In this study, we report the gut microbiota profile of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis mice treated with F. prausnitzii and its supernatant on the basis of high-throughput sequencing. We interestingly found that both F. prausnitzii and its metabolites exerted protective effects against colitis in mice, which ameliorated gut dysbiosis, with an increase in bacterial diversity and the abundance of short-chain fatty acid (SCFA)-producing bacteria and a decrease in serum TNF-α and the abundance of Proteinbacteria, Acidobacteria, and Bacteroidetes. These findings will provide further evidence of the anti-inflammatory effect of F. prausnitzii, which presents therapeutic potential for IBD treatment.

摘要

越来越多的研究表明,普拉梭菌(F. prausnitzii)是一种有前景的抗炎细菌,定植于肠道,且肠道微生物群失调在炎症性肠病(IBD)的发病机制中起重要作用。在本研究中,我们基于高通量测序报告了用普拉梭菌及其上清液处理的2,4,6-三硝基苯磺酸(TNBS)诱导的结肠炎小鼠的肠道微生物群概况。我们有趣地发现,普拉梭菌及其代谢产物均对小鼠结肠炎发挥保护作用,改善了肠道生态失调,细菌多样性增加,产生短链脂肪酸(SCFA)的细菌丰度增加,血清TNF-α以及变形菌门、酸杆菌门和拟杆菌门的丰度降低。这些发现将为普拉梭菌的抗炎作用提供进一步证据,其为IBD治疗展现出治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4378/7914335/b4f37dd748db/13568_2021_1197_Fig1_HTML.jpg

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