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The Effect of Ascorbic Acid on Helicobacter pylori Induced Cyclooxygenase 2 Expression and Prostaglandin E 2 Production by Gastric Epithelial Cells in vitro
Author(s) -
Smith Geoff V.,
Farthing Michael J. G.
Publication year - 2005
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/j.1523-5378.2005.00295.x
Subject(s) - helicobacter pylori , ascorbic acid , prostaglandin e2 , cyclooxygenase , prostaglandin e , prostaglandin , gastric acid , gastric mucosa , in vitro , chemistry , secretion , medicine , biology , endocrinology , stomach , biochemistry , enzyme , food science
Background. Cyclooxygenase 2 (COX‐2) is induced by the presence of Helicobacter pylori ( H. pylori ) on the gastric mucosa as part of the inflammatory response; this results in the synthesis of prostaglandins that amplify the local inflammatory response. The presence of H. pylori inhibits the secretion of ascorbate into the gastric lumen. Interestingly, ascorbate inhibits the growth of H. pylori and low dietary levels are associated with an increased risk of gastric adenocarcinoma. We therefore investigated the effect of ascorbate on H. pylori mediated COX‐2 induction and prostaglandin production in vitro . Methods. H. pylori was cocultured with gastric epithelial cells in the presence of ascorbate at physiological concentrations. The expression of COX‐2 was assessed by Western blotting and prostaglandin E 2 (PGE 2 ) was assessed by ELISA. Results. Ascorbate inhibited gastric cell PGE 2 synthesis but not in COX‐2 expression in response to H. pylori . In the absence of the organism, ascorbate also reduced PGE 2 expression in cells that constitutively express COX‐2, again with no reduction of COX‐2 protein expression. Conclusions. Physiological concentrations of ascorbate inhibit PGE 2 but not COX‐2 expression in response to H. pylori in gastric epithelial cells.