Copyright
©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
Expression of Interleukin-26 is upregulated in inflammatory bowel disease
Makoto Fujii, Atsushi Nishida, Hirotsugu Imaeda, Masashi Ohno, Kyohei Nishino, Shigeki Sakai, Osamu Inatomi, Shigeki Bamba, Masahiro Kawahara, Tomoharu Shimizu, Akira Andoh
Makoto Fujii, Atsushi Nishida, Hirotsugu Imaeda, Masashi Ohno, Kyohei Nishino, Shigeki Sakai, Osamu Inatomi, Shigeki Bamba, Masahiro Kawahara, Akira Andoh, Department of Medicine, Shiga University of Medical Science, Seta-Tsukinowa, Otsu 520-2192, Japan
Tomoharu Shimizu, Department of Surgery, Shiga University of Medical Science, Seta-Tsukinowa, Otsu 520-2192, Japan
Author contributions: Fujii M and Nishida A performed the majority of experiments and analyzed the data; Imaeda H, Nishino K, Sakai S, Inatomi O, Bamba S, Kawahara M, Shimizu T and Andoh A coordinated the research and provided technical support; Fujii M, Nishida A and Andoh A wrote the paper.
Institutional review board statement: This study was reviewed and approved by the local ethics committee of the Shiga University of Medical Science (Permit number: 27-27).
Conflict-of-interest statement: The authors declare that they have no competing interests.
Data sharing statement: No additional data are available.
Open-Access: 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. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Atsushi Nishida, MD, PhD, Department of Medicine, Shiga University of Medical Science, Seta Tsukinowa, Otsu 520-2192, Japan. atsuda@belle.shiga-med.ac.jp
Telephone: +81-77-5482217 Fax: +81-77-5482219
Received: April 7, 2017
Peer-review started: April 10, 2017
First decision: June 8, 2017
Revised: June 26, 2017
Accepted: July 12, 2017
Article in press: July 12, 2017
Published online: August 14, 2017
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.
Core tip: We investigated interleukin (IL)-26 expression in the inflamed mucosa of patients with inflammatory bowel disease (IBD) and characterized the biological function of IL-26 using human colonic subepithelial myofibroblasts. To our knowledge, this is the first report to state that IL-26 activates STAT1/3 and leads to the induction of IL-6 and IL-8 expression in non-transformed cells derived from human colon. We suggest that IL-26 plays a role in the pathophysiology of IBD through the induction of inflammatory mediators.
