黄芪多糖诱导的肠道微生物群在增强肉鸡肠道屏障功能方面发挥着主导作用。

IF 6.3 Q1 AGRICULTURE, DAIRY & ANIMAL SCIENCE
Jiantao Yang, Yanpeng Sun, Qianggang Wang, Shanglin Yu, Yanhe Li, Bin Yao, Xiaojun Yang
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引用次数: 0

摘要

背景:肠道屏障是抵御病原体和外来抗原入侵肠道的第一道防线,与肠道微生物群密切相关。黄芪多糖(APS)具有保护肠道屏障功能的作用,因此在传统中药中有着悠久的使用历史。APS诱导肠道微生物群增强肠道屏障功能的机制亟待研究:结果:日粮多糖剥夺诱导肠道屏障功能障碍、生长性能下降、微生物组成(粪杆菌、多拉菌和铜绿菌)改变和异丁酸浓度降低。结果表明,APS 可促进肉鸡肠道屏障功能,包括粘液层变厚、隐窝深度降低和紧密连接蛋白的生长。我们研究了 APS 诱导的肠道微生物区系,发现 APS 选择性地促进了 Parabacteroides 的生长,这是一种共生菌,在增强肠道屏障功能方面发挥着主要作用。体外生长试验进一步证实,APS 可选择性地增加副乳杆菌(Parabacteroides distasonis)和均匀乳杆菌(Bacteroides uniformis)的丰度。膳食中补充 APS 增加了异丁酸盐和胆汁酸(主要是去氧胆酸和去氧胆酸)的浓度,并激活了与肠道屏障功能相关的信号通路(如内质网中的蛋白质加工、紧密连接和粘连接头信号通路):结论:APS干预通过选择性地促进膳食多糖诱导的肠屏障功能障碍,并增加异丁酸和胆汁酸(主要是CDCA和DCA)的浓度,从而恢复了肠屏障功能障碍。这些研究结果表明,APS 诱导的肠道微生物群和代谢龛位是增强肠道屏障功能的有效策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Astragalus polysaccharides-induced gut microbiota play a predominant role in enhancing of intestinal barrier function of broiler chickens.

Background: The intestinal barrier is the first line of defense against intestinal invasion by pathogens and foreign antigens and is closely associated with the gut microbiota. Astragalus polysaccharides (APS) have a long history of use in traditional Chinese medicine owing to its protective properties against intestinal barrier function. The mechanism of APS-induced gut microbiota enhancing intestinal barrier function is urgently needed.

Results: Dietary polysaccharide deprivation induced intestinal barrier dysfunction, decreased growth performance, altered microbial composition (Faecalibacterium, Dorea, and Coprobacillus), and reduced isobutyrate concentration. The results showed that APS facilitates intestinal barrier function in broiler chickens, including a thicker mucus layer, reduced crypt depth, and the growth of tight junction proteins. We studied the landscape of APS-induced gut microbiota and found that APS selectively promoted the growth of Parabacteroides, a commensal bacterium that plays a predominant role in enhancing intestinal barrier function. An in vitro growth assay further verified that APS selectively increased the abundance of Parabacteroides distasonis and Bacteroides uniformis. Dietary APS supplementation increased the concentrations of isobutyrate and bile acid (mainly chenodeoxycholic acid and deoxycholate acid) and activated signaling pathways related to intestinal barrier function (such as protein processing in the endoplasmic reticulum, tight junctions, and adherens junction signaling pathways).

Conclusions: APS intervention restored the dietary polysaccharide-induced dysfunction of the intestinal barrier by selectively promoting the abundance of Parabacteroides distasonis, and increasing the concentrations of isobutyrate and bile acids (mainly CDCA and DCA). These findings suggest that APS-induced gut microbiota and metabolic niches are promising strategies for enhancing intestinal barrier function.

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