Abnormal intestinal permeability in Crohn's disease pathogenesis

被引:75
作者
Teshima, Christopher W. [1 ]
Dieleman, Levinus A. [1 ]
Meddings, Jon B. [2 ]
机构
[1] Univ Alberta, Div Gastroenterol, Edmonton, AB, Canada
[2] Univ Calgary, Dept Med, Calgary, AB, Canada
来源
BARRIERS AND CHANNELS FORMED BY TIGHT JUNCTION PROTEINS II | 2012年 / 1258卷
关键词
Crohn's disease; experimental colitis; intestinal permeability; microbiome; pathogenesis; INFLAMMATORY-BOWEL-DISEASE; TIGHT JUNCTIONS; BARRIER; RELATIVES; HOMEOSTASIS; SIBLINGS; RELAPSE;
D O I
10.1111/j.1749-6632.2012.06612.x
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Increased small intestinal permeability is a longstanding observation in both Crohn's disease patients and in their healthy, asymptomatic first-degree relatives. However, the significance of this compromised gut barrier function and its place in the pathogenesis of the disease remains poorly understood. The association between abnormal small intestinal permeability and a specific mutation in the NOD2 gene, which functions to modulate both innate and adaptive immune responses to intestinal bacteria, suggests a common, genetically determined pathway by which an abnormal gut barrier could result in chronic intestinal inflammation. Furthermore, rodent colitis models show that gut barrier defects precede the development of inflammatory changes. However, it remains possible that abnormal permeability is simply a consequence of mucosal inflammation. Further insight into whether abnormal barrier function is the cause or consequence of chronic intestinal inflammation will be crucial to understanding the role of intestinal permeability in the pathogenesis of Crohn's disease.
引用
收藏
页码:159 / 165
页数:7
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