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Science. 2003 May 30;300(5624):1430-4.

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

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1
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA. amieva@stanford.edu

Abstract

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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PMID:
12775840
PMCID:
PMC3369828
DOI:
10.1126/science.1081919
[Indexed for MEDLINE]
Free PMC Article

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