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PD-1 deficiency protects experimental colitis via alteration of gut microbiota
SEONG JEONG PARK1, JI-HAE KIM1, MI-YOUNG SONG2, YOUNG CHUL SUNG1,2, SEUNG-WOO LEE1,2,*,#, YUNJI PARK2,#
1Department of Life Sciences and 2Division of Integrative Biosciences and Biotechnology, POSTECH
Abstract
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 the 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. Moreover, 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 the altered bacterial communities of colon.
Abstract, Accepted Manuscript(in press) [Submitted on August 23, 2017, Accepted on September 22, 2017]
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