IL-1R2 deficiency suppresses dextran sodium sulfate-induced colitis in mice via regulation of microbiota

Biochem Biophys Res Commun. 2018 Feb 12;496(3):934-940. doi: 10.1016/j.bbrc.2018.01.116. Epub 2018 Feb 2.

Abstract

Ulcerative colitis (UC) is an inflammatory disease of the colon. IL1R2, which encodes IL-1 receptor type 2 (IL-1R2), was reported as a risk gene for UC. To elucidate the roles of IL-1R2 in the development of colitis, we examined the development of dextran sodium sulfate-induced colitis, a mouse model for UC using Il1r2-/- mice. We found the severity score of colitis was milder in Il1r2-/- mice compared with wild-type (WT) mice when they were housed separately, however the severity score was similar when they were housed in a cage. In the separate housing condition, relative contents of Actinobacteria and Bacilli in feces of Il1r2-/- mice were lower than that of WT mice. Furthermore, IL-1β induced the expression of antimicrobial peptides (AMPs) from colon. Thus, we show that IL-1R2 is harmful for the development of colitis, because IL-1R2 promotes the growth of proinflammatory intestinal microbiota by suppressing IL-1β-induced AMP production.

Keywords: Colitis; IL-1R2; Microbiota.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antimicrobial Cationic Peptides / immunology*
  • Colitis / chemically induced
  • Colitis / immunology*
  • Colitis / pathology
  • Dextran Sulfate
  • Female
  • Gastrointestinal Microbiome / immunology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Receptors, Interleukin-1 / genetics
  • Receptors, Interleukin-1 / immunology*

Substances

  • Antimicrobial Cationic Peptides
  • Receptors, Interleukin-1
  • interleukin-36 receptor, mouse
  • Dextran Sulfate