[논문]PD-1 deficiency protects experimental colitis via alteration of gut microbiota

Park, Seong Jeong; Kim, Ji-Hae; Song, Mi-Young; Sung, Young Chul; Lee, Seung-Woo; Park, Yunji

doi:10.5483/bmbrep.2017.50.11.165

[국내논문] PD-1 deficiency protects experimental colitis via alteration of gut microbiota 원문보기

BMB reports, v.50 no.11, 2017년, pp.578 - 583

Park, Seong Jeong (Department of Life Sciences, Pohang University of Science and Technology) , Kim, Ji-Hae (Department of Life Sciences, Pohang University of Science and Technology) , Song, Mi-Young (Division of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology) , Sung, Young Chul (Department of Life Sciences, Pohang University of Science and Technology) , Lee, Seung-Woo (Department of Life Sciences, Pohang University of Science and Technology) , Park, Yunji (Division of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology)

Abstract ▼ AI-Helper

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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대상 데이터

Specific-pathogen-free C57BL/6 (B6) mice were purchased from The Jackson Laboratory (Bar Harbor, ME). PD-1^−/− mice in B6-background were obtained from Dr.
Sang-Nae Cho (Yonsei University, Korea). Mice were bred and maintained in the animal facility at the Pohang University of Science and Technology Biotech Center (Pohang, Korea), and 6- to 10-wk-old mice were used for all experiments. To induce colitis, B6 or PD-1^−/− mice were fed with 2% (w/v) dextran sulfate sodium (DSS; m.

데이터처리

*P ＜ 0.05, **P ＜ 0.01 vs. DSS (-), WT mice; †P ＜ 0.05, ††P ＜ 0.01 vs. DSS (+), PD-1−/− mice by Student’s t-test.
*P ＜ 0.05, **P ＜ 0.01 vs. single housed controls and †P ＜ 0.05 vs. WT, cohoused controls by Student’s t-test.
Data are representative of two independent experiments with similar results **P ＜ 0.01, ***P ＜ 0.0001 by Student’s t-test.
Differences between the groups were assessed using two-tailed Student’s t-test.

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