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Medina-Contreras, Oscar; Harusato, Akihito; Nishio, Hikaru; Flannigan, Kyle L; Ngo, Vu; Leoni, Giovanna; Neumann, Philipp-Alexander; Geem, Duke; Lili, Loukia N; Ramadas, Ravisankar A; Chassaing, Benoit; Gewirtz, Andrew T; Kohlmeier, Jacob E; Parkos, Charles A; Towne, Jennifer E; Nusrat, Asma; Denning, Timothy L
The Journal of immunology (1950), 2016-Jan-01, 2016-01-01, 20160101, Volume: 196, Issue: 1Journal Article
IL-1 family members are central mediators of host defense. In this article, we show that the novel IL-1 family member IL-36γ was expressed during experimental colitis and human inflammatory bowel disease. Germ-free mice failed to induce IL-36γ 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.
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