Disruption of the epithelial apical-junctional complex by Helicobacter pylori CagA

被引：577
作者：
Amieva, MR [1 ]
Vogelmann, R
Covacci, A
Tompkins, LS
Nelson, WJ
Falkow, S
机构：
[1] Stanford Univ, Sch Med, Dept Microbiol & Immunol, Stanford, CA 94305 USA
[2] Stanford Univ, Sch Med, Dept Pediat, Stanford, CA 94305 USA
[3] Stanford Univ, Sch Med, Dept Cellular & Mol Physiol, Stanford, CA 94305 USA
[4] Stanford Univ, Sch Med, Dept Med, Stanford, CA 94305 USA
[5] Ist Ric Immunobiol Siena Chiron Vaccines, I-53100 Siena, Italy
来源：
SCIENCE | 2003年 / 300卷 / 5624期
关键词：
D O I：
10.1126/science.1081919
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：
Helicobacter pylori translocates the protein CagA into gastric epithelial cells and has been linked to peptic ulcer disease and gastric carcinoma. We show that injected CagA associates with the epithelial tight-junction scaffolding protein ZO-1 and the transmembrane protein junctional adhesion molecule, causing an ectopic assembly of tight-junction components at sites of bacterial attachment, and altering the composition and function of the apical-junctional complex. Long-term CagA delivery to polarized epithelia caused a disruption of the epithelial barrier function and dysplastic alterations in epithelial cell morphology. CagA appears to target H. pylori to host cell intercellular junctions and to disrupt junction-mediated functions.
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页码：1430 / 1434
页数：6
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