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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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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
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author Fujii, Makoto
Nishida, Atsushi
Imaeda, Hirotsugu
Ohno, Masashi
Nishino, Kyohei
Sakai, Shigeki
Inatomi, Osamu
Bamba, Shigeki
Kawahara, Masahiro
Shimizu, Tomoharu
Andoh, Akira
author_facet Fujii, Makoto
Nishida, Atsushi
Imaeda, Hirotsugu
Ohno, Masashi
Nishino, Kyohei
Sakai, Shigeki
Inatomi, Osamu
Bamba, Shigeki
Kawahara, Masahiro
Shimizu, Tomoharu
Andoh, Akira
author_sort Fujii, Makoto
collection PubMed
description 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.
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spelling pubmed-55581152017-08-29 Expression of Interleukin-26 is upregulated in inflammatory bowel disease Fujii, Makoto Nishida, Atsushi Imaeda, Hirotsugu Ohno, Masashi Nishino, Kyohei Sakai, Shigeki Inatomi, Osamu Bamba, Shigeki Kawahara, Masahiro Shimizu, Tomoharu Andoh, Akira World J Gastroenterol Basic Study 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. Baishideng Publishing Group Inc 2017-08-14 2017-08-14 /pmc/articles/PMC5558115/ /pubmed/28852311 http://dx.doi.org/10.3748/wjg.v23.i30.5519 Text en ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved. http://creativecommons.org/licenses/by-nc/4.0/ This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.
spellingShingle Basic Study
Fujii, Makoto
Nishida, Atsushi
Imaeda, Hirotsugu
Ohno, Masashi
Nishino, Kyohei
Sakai, Shigeki
Inatomi, Osamu
Bamba, Shigeki
Kawahara, Masahiro
Shimizu, Tomoharu
Andoh, Akira
Expression of Interleukin-26 is upregulated in inflammatory bowel disease
title Expression of Interleukin-26 is upregulated in inflammatory bowel disease
title_full Expression of Interleukin-26 is upregulated in inflammatory bowel disease
title_fullStr Expression of Interleukin-26 is upregulated in inflammatory bowel disease
title_full_unstemmed Expression of Interleukin-26 is upregulated in inflammatory bowel disease
title_short Expression of Interleukin-26 is upregulated in inflammatory bowel disease
title_sort expression of interleukin-26 is upregulated in inflammatory bowel disease
topic Basic Study
url 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
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