Induction of COX-2 expression by Helicobacter pylori is mediated by


pylori is mediated by activation of epidermal growth factor recep-tor in gastric epithelial cells. Am J Physiol Gastrointest Liver Physiol 305: G196 –G203, 2013. First published May 16, 2013; doi:10.1152/ajpgi.00495.2012.—Chronic infection of the gastric mucosa by Helicobacter pylori is associated with an increased risk of developing gastric cancer; however, the vast majority of infected individuals never develop this disease. One H. pylori virulence factor that increases gastric cancer risk is the cag pathogenicity island, which encodes a bacterial type IV secretion system. Cyclooxygenase-2 (COX-2) expression is induced by proinflammatory stimuli, leading to increased prostaglandin E2 (PGE2) secretion by gastric epithelial cells. COX-2 expression is increased in gastric tissue from H. pylori-infected persons. H. pylori also activates the epidermal growth factor receptor (EGFR) in gastric epithelial cells. We now demonstrate that H. pylori-induced activation of COX-2 in gastric cells is dependen

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