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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...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Baishideng Publishing Group Inc
2017
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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. |
format | Online Article Text |
id | pubmed-5558115 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Baishideng Publishing Group Inc |
record_format | MEDLINE/PubMed |
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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