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© Benoît Chassaing
Interaction microbiote-mucus à la surface de l’épithélium colique humain
Publication : Journal of immunology (Baltimore, Md. : 1950)

Cutting Edge: IL-36 Receptor Promotes Resolution of Intestinal Damage.

Team: Microbiome-Host Interactions
Team: U1306 – Host-Microbe interactions and pathophysiology
Member: Benoit Chassaing
Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Journal of immunology (Baltimore, Md. : 1950) - 01 Jan 2016

Medina-Contreras O, Harusato A, Nishio H, Flannigan KL, Ngo V, Leoni G, Neumann PA, Geem D, Lili LN, Ramadas RA, Chassaing B, Gewirtz AT, Kohlmeier JE, Parkos CA, Towne JE, Nusrat A, Denning TL

Link to Pubmed [PMID] – 26590314

Link to DOI – 10.4049/jimmunol.1501312

J Immunol 2016 Jan; 196(1): 34-8

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.