New insights into the dichotomous role of innate cytokines in gut homeostasis and inflammation

被引:116
作者
Bamias, Giorgos [1 ,4 ]
Corridoni, Daniele [1 ,3 ]
Pizarro, Theresa T. [2 ,3 ]
Cominelli, Fabio [1 ,3 ]
机构
[1] Case Western Reserve Univ, Dept Med, Cleveland, OH 44122 USA
[2] Case Western Reserve Univ, Dept Pathol, Cleveland, OH 44122 USA
[3] Case Western Reserve Univ, Digest Hlth Res Ctr, Cleveland, OH 44122 USA
[4] Univ Athens, Sch Med, Laikon Gen Hosp, Dept Propaedeut & Internal Med 1,GI Div, GR-11527 Athens, Greece
关键词
Cytokines; TNF superfamily; Interleukins; Intestinal inflammationl; Inflammatory bowel disease; ANTIGEN-INDUCED ARTHRITIS; DEXTRAN SULFATE SODIUM; CROHNS-DISEASE; BOWEL-DISEASE; INTESTINAL INFLAMMATION; ULCERATIVE-COLITIS; HUMAN MONOCYTES; MOUSE MODELS; RECEPTOR; TL1A;
D O I
10.1016/j.cyto.2012.06.014
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
In addition to their well-known role in acute injury and chronic inflammation, "innate" cytokines play an important role in health and the maintenance of normal immune homeostasis. This group includes the prototypic cytokines IL-1 and TNF alpha, as well as several other members belonging to the IL-1 and TNF family, such as IL-18, IL-33, IL-36-38, and TL1A. The dichotomous role of these cytokines has been best characterized in the intestine where innate cytokines may play both a protective and a pro-inflammatory role, depending upon the immmunological status of the host or the type and phase of the inflammatory process. This new information has produced novel pathogenetic hypotheses that have important translational implications both in regard to the prevention and treatment of chronic intestinal inflammation, including Crohn's disease and ulcerative colitis, the two major forms of inflammatory bowel disease. This review will discuss and summarize current data regarding the role of IL-1, TNF alpha, and their family members in regulating gut mucosal homeostasis and chronic intestinal inflammation. (C) 2012 Published by Elsevier Ltd.
引用
收藏
页码:451 / 459
页数:9
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