Disruption of the Epithelial Apical-Junctional Complex by Helicobacter pylori CagA-Reference-Cited by-同舟云学术

Disruption of the Epithelial Apical-Junctional Complex by Helicobacter pylori CagA

Published:2003-05-30 Issue:5624 Volume:300 Page:1430-1434
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Amieva Manuel R.¹²³⁴⁵,Vogelmann Roger¹²³⁴⁵,Covacci Antonello¹²³⁴⁵,Tompkins Lucy S.¹²³⁴⁵,Nelson W. James¹²³⁴⁵,Falkow Stanley¹²³⁴⁵

Affiliation:

1. Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.

2. Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305, USA.

3. Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305, USA.

4. Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.

5. Istituto Ricerche Immunobiologiche Siena–Chiron Vaccines, via Fiorentina 1, 53100 Siena, Italy.

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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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