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Expression of Interleukin-26 is upregulated in inflammatory bowel disease

AIM: To investigate interleukin (IL)-26 expression in the inflamed mucosa of patients with inflammatory bowel disease (IBD) and the function of IL-26. METHODS: Human colonic subepithelial myofibroblasts (SEMFs) were isolated from colon tissue surgically resected. The expression of IL-26 protein and...

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Detalles Bibliográficos
Autores principales: Fujii, Makoto, Nishida, Atsushi, Imaeda, Hirotsugu, Ohno, Masashi, Nishino, Kyohei, Sakai, Shigeki, Inatomi, Osamu, Bamba, Shigeki, Kawahara, Masahiro, Shimizu, Tomoharu, Andoh, Akira
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Baishideng Publishing Group Inc 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5558115/
https://www.ncbi.nlm.nih.gov/pubmed/28852311
http://dx.doi.org/10.3748/wjg.v23.i30.5519
Descripción
Sumario:AIM: To investigate interleukin (IL)-26 expression in the inflamed mucosa of patients with inflammatory bowel disease (IBD) and the function of IL-26. METHODS: Human colonic subepithelial myofibroblasts (SEMFs) were isolated from colon tissue surgically resected. The expression of IL-26 protein and its receptor complex was analyzed by immunohistochemistry. The gene expression induced by IL-26 was evaluated by real-time polymerase chain reaction. Intracellular signaling pathways were evaluated by immunoblotting and specific small interfering (si) RNA transfection. RESULTS: The mRNA and protein expression of IL-26 were significantly enhanced in the inflamed mucosa of patients with IBD. IL-26 receptor complex was expressed in colonic SEMFs in vivo and in vitro. IL-26 stimulated the mRNA expression of IL-6 and IL-8 in colonic SEMFs. The inhibitors of mitogen-activated protein kinases and phosphoinositide 3-kinase, and siRNAs for signal transducers and activator of transcription 1/3, nuclear factor-kappa B and activator protein-1 significantly reduced the mRNA expression of IL-6 and IL-8 induced by IL-26. CONCLUSION: These results suggest that IL-26 plays a role in the pathophysiology of IBD through induction of inflammatory mediators.