Expression of Interleukin-26 is upregulated in inflammatory bowel disease

被引:27
|
作者
Fujii, Makoto [1 ]
Nishida, Atsushi [1 ]
Imaeda, Hirotsugu [1 ]
Ohno, Masashi [1 ]
Nishino, Kyohei [1 ]
Sakai, Shigeki [1 ]
Inatomi, Osamu [1 ]
Bamba, Shigeki [1 ]
Kawahara, Masahiro [1 ]
Shimizu, Tomoharu [2 ]
Andoh, Akira [1 ]
机构
[1] Shiga Univ Med Sci, Dept Med, Otsu, Shiga 5202192, Japan
[2] Shiga Univ Med Sci, Dept Surg, Otsu, Shiga 5202192, Japan
关键词
inflammatory bowel disease; interleukin-26; myofibroblasts; COLONIC SUBEPITHELIAL MYOFIBROBLASTS; ULCERATIVE-COLITIS; T-CELLS; LYMPHOCYTES; RECEPTOR-2; MICROBIOTA; INDUCTION; HEALTH; IL-26; LOCI;
D O I
10.3748/wjg.v23.i30.5519
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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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页码:5519 / 5529
页数:11
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