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Lypd8 促进鞭毛菌的分离和结肠上皮的分离。

Lypd8 promotes the segregation of flagellated microbiota and colonic epithelia.

机构信息

Laboratory of Immune Regulation, Department of Microbiology and Immunology, Graduate School of Medicine, WPI Immunology Frontier Research Center, Osaka University, Suita, Osaka 565-0871, Japan.

Core Research for Evolutional Science and Technology, Japan Agency for Medical Research and Development, Tokyo 100-0004, Japan.

出版信息

Nature. 2016 Apr 7;532(7597):117-21. doi: 10.1038/nature17406. Epub 2016 Mar 30.

Abstract

Colonic epithelial cells are covered by thick inner and outer mucus layers. The inner mucus layer is free of commensal microbiota, which contributes to the maintenance of gut homeostasis. In the small intestine, molecules critical for prevention of bacterial invasion into epithelia such as Paneth-cell-derived anti-microbial peptides and regenerating islet-derived 3 (RegIII) family proteins have been identified. Although there are mucus layers providing physical barriers against the large number of microbiota present in the large intestine, the mechanisms that separate bacteria and colonic epithelia are not fully elucidated. Here we show that Ly6/PLAUR domain containing 8 (Lypd8) protein prevents flagellated microbiota invading the colonic epithelia in mice. Lypd8, selectively expressed in epithelial cells at the uppermost layer of the large intestinal gland, was secreted into the lumen and bound flagellated bacteria including Proteus mirabilis. In the absence of Lypd8, bacteria were present in the inner mucus layer and many flagellated bacteria invaded epithelia. Lypd8(-/-) mice were highly sensitive to intestinal inflammation induced by dextran sulfate sodium (DSS). Antibiotic elimination of Gram-negative flagellated bacteria restored the bacterial-free state of the inner mucus layer and ameliorated DSS-induced intestinal inflammation in Lypd8(-/-) mice. Lypd8 bound to flagella and suppressed motility of flagellated bacteria. Thus, Lypd8 mediates segregation of intestinal bacteria and epithelial cells in the colon to preserve intestinal homeostasis.

摘要

结肠上皮细胞被厚厚的内层和外层黏液层覆盖。内层黏液层中不存在共生微生物群,这有助于维持肠道内环境的稳定。在小肠中,已经鉴定出了一些对防止细菌入侵上皮组织至关重要的分子,如潘氏细胞衍生的抗菌肽和再生胰岛衍生 3(RegIII)家族蛋白。尽管存在黏液层为大肠中存在的大量微生物提供物理屏障,但将细菌与结肠上皮组织分隔开的机制尚未完全阐明。在这里,我们发现 Ly6/PLAUR 结构域包含 8(Lypd8)蛋白可防止鞭毛状微生物侵入小鼠的结肠上皮组织。Lypd8 选择性地在上层大肠腺上皮细胞中表达,分泌到腔中,并与包括奇异变形杆菌在内的鞭毛状细菌结合。在没有 Lypd8 的情况下,细菌存在于内层黏液层中,并且许多鞭毛状细菌入侵了上皮组织。Lypd8(-/-) 小鼠对葡聚糖硫酸钠(DSS)诱导的肠道炎症高度敏感。抗生素消除革兰氏阴性鞭毛状细菌可恢复内层黏液层的无细菌状态,并改善 Lypd8(-/-) 小鼠 DSS 诱导的肠道炎症。Lypd8 与鞭毛结合并抑制鞭毛状细菌的运动。因此,Lypd8 介导了肠道细菌和结肠上皮细胞的分离,以维持肠道内环境的稳定。

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