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白细胞介素-22 缺乏会改变结肠微生物群,使其具有传染性和结肠炎发生性。

IL-22 deficiency alters colonic microbiota to be transmissible and colitogenic.

机构信息

Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.

出版信息

J Immunol. 2013 May 15;190(10):5306-12. doi: 10.4049/jimmunol.1300016. Epub 2013 Apr 12.

DOI:10.4049/jimmunol.1300016
PMID:23585682
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3646987/
Abstract

IL-22 is a good candidate to play a critical role in regulating gut microbiota because it is an important inducer of antimicrobial peptides and mucins in the gut. However, whether IL-22 participates in immune homeostasis by way of modulating gut microbiota remains to be elucidated. In this study, we find, through 16S rRNA gene-pyrosequencing analysis, that healthy IL-22-deficient mice had altered colonic microbiota, notably with decreased abundance of some genera, including Lactobacillus, and increased levels of others. Mice harboring this altered microbiota exhibited more severe disease during experimentally induced colitis. Interestingly, this altered gut microbiota can be transmitted to cohoused wild-type animals along with the increased susceptibility to this colitis, indicating an important role for IL-22 in shaping the homeostatic balance between immunity and colonic microbiota for host health.

摘要

白细胞介素 22(IL-22)是调节肠道微生物群的重要候选因子,因为它是肠道中抗菌肽和粘蛋白的重要诱导剂。然而,IL-22 是否通过调节肠道微生物群来参与免疫稳态仍有待阐明。在这项研究中,我们通过 16S rRNA 基因焦磷酸测序分析发现,健康的 IL-22 缺陷型小鼠的结肠微生物群发生了改变,特别是一些属的丰度降低,包括乳杆菌属,而其他属的水平则升高。携带这种改变的微生物群的小鼠在实验性结肠炎中表现出更严重的疾病。有趣的是,这种改变的肠道微生物群可以与易感性增加一起传递给共住的野生型动物,表明 IL-22 在塑造宿主健康的免疫和结肠微生物群之间的稳态平衡方面发挥着重要作用。

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