| First Author | Medina-Contreras O | Year | 2016 |
| Journal | J Immunol | Volume | 196 |
| Issue | 1 | Pages | 34-8 |
| PubMed ID | 26590314 | Mgi Jnum | J:256644 |
| Mgi Id | MGI:6102175 | Doi | 10.4049/jimmunol.1501312 |
| Citation | Medina-Contreras O, et al. (2016) Cutting Edge: IL-36 Receptor Promotes Resolution of Intestinal Damage. J Immunol 196(1):34-8 |
| abstractText | IL-1 family members are central mediators of host defense. In this article, we show that the novel IL-1 family member IL-36gamma was expressed during experimental colitis and human inflammatory bowel disease. Germ-free mice failed to induce IL-36gamma in response to dextran sodium sulfate (DSS)-induced damage, suggesting that gut microbiota are involved in its induction. Surprisingly, IL-36R-deficient (Il1rl2(-/-)) mice exhibited defective recovery following DSS-induced damage and impaired closure of colonic mucosal biopsy wounds, which coincided with impaired neutrophil accumulation in the wound bed. Failure of Il1rl2(-/-) mice to recover from DSS-induced damage was associated with a profound reduction in IL-22 expression, particularly by colonic neutrophils. Defective recovery of Il1rl2(-/-) mice could be rescued by an aryl hydrocarbon receptor agonist, which was sufficient to restore IL-22 expression and promote full recovery from DSS-induced damage. These findings implicate the IL-36/IL-36R axis in the resolution of intestinal mucosal wounds. |
