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黏膜相关生物氢化微生物可保护模拟结肠微生物组免受高浓度多不饱和脂肪相关的应激。

Mucosa-associated biohydrogenating microbes protect the simulated colon microbiome from stress associated with high concentrations of poly-unsaturated fat.

机构信息

Center for Microbial Ecology and Technology (CMET), Ghent University, Coupure Links 653, Ghent, BE-9000, Belgium.

Laboratory for Animal Nutrition and Product Quality (Lanupro), Ghent University, Proefhoevestraat 10, Melle, BE-9090, Belgium.

出版信息

Environ Microbiol. 2017 Feb;19(2):722-739. doi: 10.1111/1462-2920.13622. Epub 2017 Jan 25.

Abstract

Polyunsaturated fatty acids (PUFAs) may affect colon microbiome homeostasis by exerting (specific) antimicrobial effects and/or interfering with mucosal biofilm formation at the gut mucosal interface. We used standardized batch incubations and the Mucosal-Simulator of the Human Microbial Intestinal Ecosystem (M-SHIME) to show the in vitro luminal and mucosal effects of the main PUFA in the Western diet, linoleic acid (LA). High concentrations of LA were found to decrease butyrate production and Faecalibacterium prausnitzii numbers dependent on LA biohydrogenation to vaccenic acid (VA) and stearic acid (SA). In faecal batch incubations, LA biohydrogenation and butyrate production were positively correlated and SA did not inhibit butyrate production. In the M-SHIME, addition of a mucosal environment stimulated biohydrogenation to SA and protected F. prausnitzii from inhibition by LA. This was probably due to the preference of two biohydrogenating genera Roseburia and Pseudobutyrivibrio for the mucosal niche. Co-culture batch incubations using Roseburia hominis and F. prausnitzii validated these observations. Correlations networks further uncovered the central role of Roseburia and Pseudobutyrivibrio in protecting luminal and mucosal SHIME microbiota from LA-induced stress. Our results confirm how cross-shielding interactions provide resilience to the microbiome and demonstrate the importance of biohydrogenating, mucosal bacteria for recovery from LA stress.

摘要

多不饱和脂肪酸(PUFAs)可能通过发挥(特定)抗菌作用和/或干扰肠道黏膜界面的黏膜生物膜形成来影响结肠微生物组稳态。我们使用标准化批量孵育和人类微生物肠道生态系统黏膜模拟器(M-SHIME)来显示西方饮食中主要多不饱和脂肪酸亚油酸(LA)的腔内和黏膜效应。发现高浓度的 LA 降低了但丁酸盐的产生和普拉梭菌的数量,这取决于 LA 的生物氢化生成壬烯酸(VA)和硬脂酸(SA)。在粪便批量孵育中,LA 的生物氢化和丁酸盐的产生呈正相关,而 SA 并不抑制丁酸盐的产生。在 M-SHIME 中,添加黏膜环境刺激了 SA 的生物氢化,并保护了普拉梭菌免受 LA 的抑制。这可能是由于两种生物氢化菌罗斯伯里氏菌和假丁酸弧菌对黏膜生态位的偏好。使用罗斯伯里氏菌和普拉梭菌的共培养批量孵育验证了这些观察结果。相关网络进一步揭示了罗斯伯里氏菌和假丁酸弧菌在保护腔内和黏膜 SHIME 微生物群免受 LA 诱导的应激中的核心作用。我们的结果证实了交叉屏蔽相互作用如何为微生物组提供弹性,并证明了生物氢化、黏膜细菌从 LA 应激中恢复的重要性。

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