BACKGROUND: Cyclooxygenase 2 (COX-2) is an inducible enzyme that plays a key role in the synthesis of prostaglandins in response to inflammatory stimuli. It is expressed in the gastric mucosa as part of the response to infection with Helicobacter pylori. The specific interaction between H. pylori and the gastric epithelium that results in COX-2 expression has not been identified. METHODS: In order to investigate the hypothesis that lipopolysaccharide (LPS) from H. pylori plays a role in the induction of cyclooxygenase 2 in the stomach, gastric cell lines MKN-7 and MKN-45 were incubated with LPS from either H. pylori NCTC 11637 or Escherichia coli 055:B5. Incubation of cells with live H. pylori NCTC 11637 was also carried out as a positive control. Cells were then analysed for COX-2 protein and mRNA and prostaglandin E2 synthesis. RESULTS: Cyclooxygenase 2 protein and mRNA expression was induced by E. coli LPS and live H. pylori, but not by H. pylori LPS. Prostaglandin E2 synthesis increased in a dose-dependent manner in both cell lines with E. coli but not H. pylori LPS. CONCLUSIONS: H. pylori LPS is of low biological activity when compared with E. coli LPS in its ability to induce the expression of cyclooxygenase 2 and synthesis of prostaglandin E2. This may provide one mechanism by which H. pylori minimizes the inflammatory response in the gastric mucosa, allowing chronic infection.
BACKGROUND: Cyclooxygenase 2 (COX-2) is an inducible enzyme that plays a key role in the synthesis of prostaglandins in response to inflammatory stimuli. It is expressed in the gastric mucosa as part of the response to infection with Helicobacter pylori. The specific interaction between H. pylori and the gastric epithelium that results in COX-2 expression has not been identified. METHODS: In order to investigate the hypothesis that lipopolysaccharide (LPS) from H. pylori plays a role in the induction of cyclooxygenase 2 in the stomach, gastric cell lines MKN-7 and MKN-45 were incubated with LPS from either H. pylori NCTC 11637 or Escherichia coli 055:B5. Incubation of cells with live H. pylori NCTC 11637 was also carried out as a positive control. Cells were then analysed for COX-2 protein and mRNA and prostaglandin E2 synthesis. RESULTS: Cyclooxygenase 2 protein and mRNA expression was induced by E. coli LPS and live H. pylori, but not by H. pylori LPS. Prostaglandin E2 synthesis increased in a dose-dependent manner in both cell lines with E. coli but not H. pylori LPS. CONCLUSIONS:H. pylori LPS is of low biological activity when compared with E. coli LPS in its ability to induce the expression of cyclooxygenase 2 and synthesis of prostaglandin E2. This may provide one mechanism by which H. pylori minimizes the inflammatory response in the gastric mucosa, allowing chronic infection.