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

BMB Rep. 2017 Nov;50(11):578-583. doi: 10.5483/bmbrep.2017.50.11.165.

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 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. [BMB Reports 2017; 50(11): 578-583].

Publication types

  • News

MeSH terms

  • Animals
  • Bacteria / genetics
  • Colitis / chemically induced
  • Colitis / metabolism*
  • Colitis / pathology
  • Colitis / prevention & control*
  • Colon / pathology
  • Cytokines / metabolism
  • Disease Models, Animal
  • Gastrointestinal Microbiome / physiology
  • Inflammatory Bowel Diseases / metabolism
  • Metagenomics / methods
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Programmed Cell Death 1 Ligand 2 Protein / genetics
  • Programmed Cell Death 1 Ligand 2 Protein / metabolism*
  • RNA, Ribosomal, 16S / genetics

Substances

  • Cytokines
  • Pdcd1lg2 protein, mouse
  • Programmed Cell Death 1 Ligand 2 Protein
  • RNA, Ribosomal, 16S