Epithelial barrier defects in HT-29/B6 colonic cell monolayers induced by tumor necrosis factor-α

被引:0
作者
Gitter, AH [1 ]
Bendfeldt, K
Schmitz, H
Schulzke, JD
Bentzel, CJ
Fromm, M
机构
[1] Free Univ Berlin, Klinikum Benjamin Franklin, Inst Klin Physiol, D-12200 Berlin, Germany
[2] Free Univ Berlin, Klinikum Benjamin Franklin, Med Klin 1, D-12200 Berlin, Germany
[3] E Carolina Univ, Dept Med, Greenville, NC 27858 USA
来源
EPITHELIAL TRANSPORT AND BARRIER FUNCTION: PATHOMECHANISMS IN GASTROINTESTINAL DISORDERS | 2000年 / 915卷
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D O I
暂无
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
The barrier function of intestinal epithelia relies upon the continuity of the enterocyte monolayer and intact tight junctions. After incubation with tumor necrosis factor-alpha TNF-alpha, however, the number of strands that form the tight junctions decreases, and apoptosis is induced in intestinal epithelial cells. These morphological changes lead to a rise of transepithelial ion permeability, because the paracellular ion permeability increases and leaks associated with sites of apoptosis increase by number and magnitude. Thus apoptosis and degradation of tight junctions contribute to the increased permeability observed after exposure to TNF-alpha:. These mechanisms explain clinical manifestations in the inflamed intestinal wall containing cytokine-secreting macrophages for example, leak flux diarrhea and invasion of bacterial enterotoxins.
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页码:193 / 203
页数:11
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