Stomach infection by Helicobacter pylori — a Gram-negative, flagellated bacterium — can lead to gastroduodenal inflammation, peptic ulcers and gastric carcinoma. The pathogen is known to translocate the protein CagA into gastric epithelial cells and to adhere to host cells close to the apical-junctional complex, a network of structural and signaling proteins that controls epithelial proliferation, differentiation, and barrier function.

In the May 30 Science, Manuel Amieva and colleagues at Stanford University School of Medicine link these two pieces of evidence, showing that CagA associates with the apical-junctional complex and alters its composition and function in a manner that may help explain H. pylori pathogenesis (Science, 300:1430-1434, May 30, 2003).

Amieva et al. developed a system that allowed H. pylori infection of polarized monolayers of Madin-Darby canine kidney (MDCK) cells. Bacteria targeted intracellular junctions and also recruited the tight-junction scaffolding protein ZO-1, altering its distribution. Using MDCK...

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