Tough on the Stomach

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Science  07 Mar 2003:
Vol. 299, Issue 5612, pp. 1487-1489
DOI: 10.1126/science.299.5612.1487e

About half of the world's population is infected with Helicobacter pylori, a bacterial pathogen that can cause stomach ulcers. A major virulence factor in ulcer formation is the bacterial toxin VacA, which appears to disrupt gastric epithelial cell integrity in multiple ways, including alteration of endolysosomal function, enhancement of paracellular permeability, pore formation in the plasma membrane, and apoptosis.

Fujikawa et al. describe a new cellular pathway through which VacA may exert its pathogenic effects. VacA-induced gastric injury in mice was found to require Ptprz, a host-encoded protein tyrosine phosphatase receptor expressed on gastric epithelial cells. In an in vitro model, binding of VacA to Ptprz caused epithelial cells to detach from the basement membrane, suggesting that ulcers may form because the interaction of these proteins exposes the denuded gastric mucosa to the acidic contents of the stomach. Further study of the cellular pathways affected by VacA will likely facilitate the development of vaccines and diagnostic tests for identifying individuals with a high risk of gastric disease. — PAK

Nature Genet. 10.1038/ng1112 (2003).

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