Translocation of Helicobacter pylori CagA into Gastric Epithelial Cells by Type IV Secretion
S Odenbreit, J Püls, B Sedlmaier, E Gerland… - Science, 2000 - science.org
S Odenbreit, J Püls, B Sedlmaier, E Gerland, W Fischer, R Haas
Science, 2000•science.orgThe 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 …
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 …
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 cagpathogenicity 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 chronicHelicobacter infection with yet unknown consequences.
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