Neutralization of IL-6 and TNF-α ameliorates intestinal permeability in DSS-induced colitis

被引：144
|
作者：
Xiao, Yong-Tao [1 ,2 ,3 ]
Yan, Wei-Hui [1 ,3 ]
Cao, Yi [1 ]
Yan, Jun-Kai [2 ,3 ]
Cai, Wei [1 ,2 ,3 ]
机构：
[1] Shanghai Jiao Tong Univ, Sch Med, Xin Hua Hosp, Dept Pediat Surg, Shanghai 200030, Peoples R China
[2] Shanghai Inst Pediat Res, Shanghai, Peoples R China
[3] Shanghai Key Lab Pediat Gastroenterol & Nutr, Shanghai, Peoples R China
来源：
CYTOKINE | 2016年 / 83卷
基金：
中国国家自然科学基金;
关键词：
TNF-alpha; IL-6; Dextran sulfate sodium; MLCK; Claudin-2; INFLAMMATORY-BOWEL-DISEASE; BARRIER FUNCTION; CROHNS-DISEASE; EXPRESSION; ANTIBODY; MICE;
D O I：
10.1016/j.cyto.2016.04.012
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) have been implicated as important mediators of the inflammatory reaction in patients with intestinal inflammation. The present study was designed to investigate the roles of these cytokines on mucosal barrier function in a mouse model of acute colitis with using anti-cytokine strategies. Mice received 3% dextran sulfate sodium (DSS) in their drinking water for 7 days showed morphological alteration of mucosa and increase of intestinal permeability. Administration of IL-6 monoclonal antibody (mAb) or TNF-alpha mAb significantly attenuated intestinal permeability. IL-6 mAb and TNF-a mAb treatment also effectively suppressed the expression of claudin-2 and myosin light chain kinase (MLCK). Taken together, we indicated that anti-IL-6 and anti-TNF-alpha therapy prevent intestinal permeability induced by intestinal inflammation. (C) 2016 Elsevier Ltd. All rights reserved.
引用
收藏
页码：189 / 192
页数：4
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