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World J Gastroenterol. 2017 Aug 14;23(30):5519-5529. doi: 10.3748/wjg.v23.i30.5519.

Expression of Interleukin-26 is upregulated in inflammatory bowel disease.

Author information

1
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.

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.

KEYWORDS:

Inflammatory bowel disease; Interleukin-26; Myofibroblasts

PMID:
28852311
PMCID:
PMC5558115
DOI:
10.3748/wjg.v23.i30.5519
[Indexed for MEDLINE]
Free PMC Article

Conflict of interest statement

Conflict-of-interest statement: The authors declare that they have no competing interests.

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