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New insights in gut microbiota and mucosal immunity of the small intestine

机译:小肠肠道菌群和粘膜免疫的新见解

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Beyond host genetics, the environment determines microbiota-immunity interactions. Most recent studies have focused on the interconnections between micronutrients, microbial and immune populations. However, the control of the gut oxidative stress and redox status has been neglected. Oxidative stress sensitive (Ox-S) prokaryotes include butyrate producers and minority mucosa-associated immunogenic symbionts, such as specific Lactobacillus strains, Bifidobacterium adolescentis , and segmented filamentous bacteria which exemplify the mucosal “minority report” paradigm. Butyrate, produced by Lachnospiraceae , Ruminococcaceae and Bacteroidetes , is the main microbiota-derived gut mucosal immunity regulator and the best functional marker of the healthy mature anaerobic gut microbiota (HMAGM). Oxidative stress during the “window of opportunity” around weaning is observed in severe acute malnutrition and results in Ox-S prokaryote depletion, HMAGM disruption, collapse of butyrate production and durable gut mucosal immunity alteration. High saturated-fat diet leads to oxidative stress, selection of oxidative stress-resistant (Ox-R) Lactobacillus reuteri strains in Peyer’s patches, secretion of pro-inflammatory cytokines, disruption of mucosal immune compartmentalization (leaky gut) and obesity. Beyond dietary micronutrient diversity and pathogen control, future research should focus on antioxidants, control of oxidative stress and Ox-S gut prokaryote preservation as new instrumental targets for maintenance of the gut microbiota-immunity symbiotic loop and prevention of malnutrition and obesity.
机译:除了宿主遗传学外,环境还决定了微生物与免疫的相互作用。最新研究集中在微量营养素,微生物和免疫种群之间的相互联系。然而,对肠道氧化应激和氧化还原状态的控制已被忽略。氧化应激敏感(Ox-S)原核生物包括丁酸酯生产者和少数与粘膜相关的免疫原性共生体,例如特定的乳酸菌菌株,青春双歧杆菌和分段的丝状细菌,它们是粘膜“少数群体报告”范式的例证。 Lachnospiraceae,Ruminococcaceae和Bacteroidetes产生的丁酸盐是主要的微生物群来源的肠道粘膜免疫调节剂,也是健康成熟的厌氧性肠道菌群(HMAGM)的最佳功能标记。在严重的急性营养不良中,观察到断奶期间“机会之窗”期间的氧化应激,导致Ox-S原核生物耗竭,HMAGM破坏,丁酸产量下降和肠道粘膜免疫力持久改变。高饱和脂肪饮食会导致氧化应激,在派伊尔斑中选择抗氧化应激(Ox-R)的罗伊氏乳杆菌菌株,促炎性细胞因子的分泌,粘膜免疫区室化(渗漏的肠道)和肥胖症。除了饮食中微量营养素的多样性和病原体控制之外,未来的研究应集中在抗氧化剂,氧化应激的控制和Ox-S肠道原核生物的保存,作为维持肠道微生物群-免疫共生循环和预防营养不良和肥胖的新工具。

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