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壳寡糖(COS)及其供体鼠 FMT 对肠道屏障功能和细胞凋亡的影响。

Effects of chitosan oligosaccharides (COS) and FMT from COS-dosed mice on intestinal barrier function and cell apoptosis.

机构信息

College of Life Science, South-Central Minzu University, No. 182, Minyuan Road, Hongshan District, Wuhan City, Hubei Province 430074, China.

Hubei Province Nutrition Chemicals Biosynthetic Engineering Technology Research Center, Wuhan 430073, China.

出版信息

Carbohydr Polym. 2022 Dec 1;297:120043. doi: 10.1016/j.carbpol.2022.120043. Epub 2022 Aug 29.

DOI:10.1016/j.carbpol.2022.120043
PMID:36184150
Abstract

Chitosan oligosaccharides (COS) show the potential to support the intestinal health, but the mechanism and role of COS-derived intestinal microbiota are unknown. We explored the protective effect of direct administration of COS on intestinal barrier function using an in vivo colitis mouse model and an in vitro enterotoxigenic Escherichia coli (ETEC)-challenged IPEC-J2 cell model. COS directly enhanced the intestinal barrier function. COS intervention also promoted the abundance and diversity of intestinal flora. Importantly, FMT intervention with a COS-derived microbiome decreased the disease index level and alleviated histopathological changes, and improved gut barrier function in the colitis model. Both COS and COS-derived microbiota suppressed ETEC-induced cellular apoptosis in IPEC-J2 cells. This study firstly confirms transplantation of COS-modified fecal microbiota can enhance the intestinal barrier function. The mechanism underlying COS benefits is due to a direct intervention by COS supplementation and an indirect improvement of the gut microbiota induced by COS exposure.

摘要

壳寡糖(COS)具有支持肠道健康的潜力,但 COS 衍生的肠道微生物群的作用机制尚不清楚。我们使用体内结肠炎小鼠模型和体外肠产毒性大肠杆菌(ETEC)攻毒 IPEC-J2 细胞模型,探索了 COS 直接给药对肠道屏障功能的保护作用。COS 直接增强了肠道屏障功能。COS 干预还促进了肠道菌群的丰度和多样性。重要的是,用源自 COS 的微生物群进行 FMT 干预降低了结肠炎模型中的疾病指数水平,减轻了组织病理学变化,并改善了肠道屏障功能。COS 和源自 COS 的微生物群均抑制了 ETEC 诱导的 IPEC-J2 细胞细胞凋亡。本研究首次证实移植经 COS 修饰的粪便微生物群可以增强肠道屏障功能。COS 发挥作用的机制归因于 COS 补充的直接干预和 COS 暴露间接改善肠道微生物群。

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