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KMID : 0624620170500110578
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BMB Reports
2017 Volume.50 No. 11 p.578 ~ p.583
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PD-1 deficiency protects experimental colitis via alteration of gut microbiota
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Park Seong-Jeong
Kim Ji-Hae
Song Mi-Young
Sung Young-Chul
Lee Seung-Woo
Park Yun-Ji
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Abstract
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Programmed cell death-1 (PD-1) is a coinhibitory molecule and plays a pivotal role in immune regulation. Here, we demonstrate a role for PD-1 in pathogenesis of inflammatory bowel disease (IBD). Wild-type (WT) mice had severe wasting disease during experimentally induced colitis, while mice deficient for PD-1 (PD-1?/?) did not develop colon inflammation. Interestingly, PD-1?/? mice cohoused with WT mice became susceptible to colitis, suggesting that resistance of PD-1?/? mice to colitis is dependent on their gut microbiota. 16S rRNA gene-pyrosequencing analysis showed that PD-1?/? mice had altered composition of gut microbiota with significant reduction in Rikenellaceae family. These altered colon bacteria of PD-1?/? mice induced less amount of inflammatory mediators from colon epithelial cells, including interleukin (IL)-6, and inflammatory chemokines. Taken together, our study indicates that PD-1 expression is involved in the resistance to experimental colitis through altered bacterial communities of colon.
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KEYWORD
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Colitis, Inflammation, Metagenomics, Microbiota, PD-1
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