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. 2000 Feb 25;287(5457):1497-500.
doi: 10.1126/science.287.5457.1497.

Translocation of Helicobacter pylori CagA into gastric epithelial cells by type IV secretion

S Odenbreit  1 , J Püls, B Sedlmaier, E Gerland, W Fischer, R Haas
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Translocation of Helicobacter pylori CagA into gastric epithelial cells by type IV secretion

S Odenbreit et al. Science. .

Abstract

The Gram-negative bacterium Helicobacter pylori is a causative agent of gastritis and peptic ulcer disease in humans. Strains producing the CagA antigen (cagA(+)) induce strong gastric inflammation and are strongly associated with gastric adenocarcinoma and MALT lymphoma. We show here that such strains translocate the bacterial protein CagA into gastric epithelial cells by a type IV secretion system, encoded by the cag pathogenicity island. CagA is tyrosine-phosphorylated and induces changes in the tyrosine phosphorylation state of distinct cellular proteins. Modulation of host cells by bacterial protein translocation adds a new dimension to the chronic Helicobacter infection with yet unknown consequences.

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