| Literature DB >> 26590314 |
Oscar Medina-Contreras1, Akihito Harusato1, Hikaru Nishio2, Kyle L Flannigan1, Vu Ngo1, Giovanna Leoni2, Philipp-Alexander Neumann2, Duke Geem3, Loukia N Lili2, Ravisankar A Ramadas4, Benoit Chassaing1, Andrew T Gewirtz1, Jacob E Kohlmeier5, Charles A Parkos6, Jennifer E Towne7, Asma Nusrat6, Timothy L Denning8.
Abstract
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.Entities:
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Year: 2015 PMID： 26590314 PMCID： PMC4684965 DOI： 10.4049/jimmunol.1501312
Source DB: PubMed Journal: J Immunol ISSN： 0022-1767 Impact factor: 5.422