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. 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). 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.

中文翻译：

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黄芪多糖诱导的肠道菌群在增强肉鸡肠道屏障功能中发挥主导作用


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，与肠道菌群密切相关。黄芪多糖（APS）因其对肠道屏障功能的保护特性而在中药中使用有着悠久的历史。迫切需要了解 APS 诱导的肠道微生物群增强肠道屏障功能的机制。膳食多糖剥夺会导致肠道屏障功能障碍、生长性能下降、微生物组成改变（粪杆菌、Dorea 和粪杆菌）以及异丁酸浓度降低。结果表明，APS 促进肉鸡肠道屏障功能，包括增厚粘液层、减少隐窝深度以及紧密连接蛋白的生长。我们研究了 APS 诱导的肠道微生物群景观，发现 APS 选择性促进副拟杆菌的生长，这是一种在增强肠道屏障功能中起主要作用的共生细菌。体外生长试验进一步证实APS选择性增加了Parabacteroides distasonis和Bacteroidesuniformis的丰度。膳食APS补充增加了异丁酸和胆汁酸（主要是鹅去氧胆酸和脱氧胆酸）的浓度，并激活了与肠道屏障功能相关的信号通路（例如内质网中的蛋白质加工、紧密连接和粘附连接信号通路）。 APS干预通过选择性促进Parabacteroides distasonis的丰度并增加异丁酸和胆汁酸（主要是CDCA和DCA）的浓度来恢复膳食多糖引起的肠道屏障功能障碍。 这些发现表明，APS 诱导的肠道微生物群和代谢生态位是增强肠道屏障功能的有前途的策略。