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

IL-22 deficiency alters colonic microbiota to be transmissible and colitogenic.
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DOI:
10.4049/jimmunol.1300016
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发表时间:
2013-05-15
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
通讯作者:
Flavell RA
Flavell RA
中科院分区:
其他
文献类型:
--
作者:
Zenewicz LA;Yin X;Wang G;Elinav E;Hao L;Zhao L;Flavell RA

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白细胞介素-22(IL-22)是调节肠道微生物群的一个很好的候选者,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参与免疫稳态仍有待阐明。在这项研究中,我们通过16 S rRNA基因焦磷酸测序分析发现,健康的IL-22缺陷小鼠改变了结肠微生物群,特别是包括乳酸杆菌在内的一些属的丰度降低,其他属的水平增加。携带这种改变的微生物群的小鼠在实验诱导的结肠炎期间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沿着共同圈养的野生型动物对这种结肠炎的易感性增加,这表明IL-22在塑造免疫和结肠微生物群之间的稳态平衡以促进宿主健康方面具有重要作用。
Interleukin-22 (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 into 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 co-housed wild-type animals along with the increased susceptibility to this colitis, indicating an important role of IL-22 in shaping the homeostatic balance between immunity and colonic microbiota for host health.
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