| First Author | Yoshida K | Year | 2018 |
| Journal | Biochem Biophys Res Commun | Volume | 496 |
| Issue | 3 | Pages | 934-940 |
| PubMed ID | 29366788 | Mgi Jnum | J:273598 |
| Mgi Id | MGI:6276812 | Doi | 10.1016/j.bbrc.2018.01.116 |
| Citation | Yoshida K, et al. (2018) IL-1R2 deficiency suppresses dextran sodium sulfate-induced colitis in mice via regulation of microbiota. Biochem Biophys Res Commun 496(3):934-940 |
| abstractText | 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-1beta 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-1beta-induced AMP production. |
