Helicobacter infection and phospholipase A(2) enzymes: Effect of Helicobacter felis-infection on the expression and activity of sPLA(2) enzymes in mouse stomach

The murine gastric mucosa possesses very high secretory type phospholipase A(2) activity. Northern and Western blots indicated that the pancreatic-typ e, sPLA(2)-IB represents the predominant form of sPLA(2) enzymes present in the gastric mucosa. Both sPLA(2)-IB mRNA and protein in the gastric mucosa exceeded levels found in the pancreas, and in contrast to the pancreatic e nzyme it was present primarily in the active state. The sPLA(2)-IB gene is not expressed in the murine small intestine and colon. Infection by the gas tritis-inducing bacteria, Helicobacter felis (H. felis) dramatically and ti me dependently decreased the PLA(2) activity in the glandular stomach of th e mouse strain, C57BL/6, sensitive to the organism, which appeared to be re lated to a decrease in the percentage of sPLA(2)-IB present in the active f orm. This bacterial-induced reduction in PLA(2) activity was not observed i n BALB/c mice that fail to develop gastritis in response to H. felis infect ion. C57BL/6 mice do not, while BALB/c mice express, the PLA(2)-II enzyme. The H. felis-induced reduction in sPLA(2)-IB activity may weaken the gastri c barrier by reducing the local concentration of arachidonic and linoleic a cid, liberated from membrane phospholipids, the major precursors of 'cytopr otective' prostaglandins. Data presented here suggest that both sPLA(2)-IB and sPLA(2)-II enzymes may contribute to the gastric response to Helicobact er infection.