Fujii M, Nishida A, Imaeda H, Ohno M, Nishino K, Sakai S, Inatomi O, Bamba S, Kawahara M, Shimizu T, Andoh A. Expression of Interleukin-26 is upregulated in inflammatory bowel disease. World J Gastroenterol 2017; 23(30): 5519-5529 [PMID: 28852311 DOI: 10.3748/wjg.v23.i30.5519]
Corresponding Author of This Article
Atsushi Nishida, MD, PhD, Department of Medicine, Shiga University of Medical Science, Seta Tsukinowa, Otsu 520-2192, Japan. atsuda@belle.shiga-med.ac.jp
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
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/
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 Processing time: 129 Days and 10.8 Hours
Abstract
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.
