Helicobacter infection and phospholipase A2 enzymes: Effect of Helicobacter felis‐infection on the expression and activity of sPLA2 enzymes in mouse stomach

The murine gastric mucosa possesses very high secretory type phospholipase A₂ activity. Northern and Western blots indicated that the pancreatictype, sPLA₂IB represents the predominant form of sPLA₂ enzymes present in the gastric mucosa. Both sPLA₂IB mRNA and protein in the gastric mucosa exceeded levels found in the pancreas, and in contrast to the pancreatic enzyme it was present primarily in the active state. The sPLA₂IB gene is not expressed in the murine small intestine and colon. Infection by the gastritis-inducing bacteria, Helicobacter felis (H. felis) dramatically and time dependently decreased the PLA₂ activity in the glandular stomach of the mouse strain, C57BL/6, sensitive to the organism, which appeared to be related to a decrease in the percentage of sPLA₂IB present in the active form. This bacterial-induced reduction in PLA₂ activity was not observed in BALB/c mice that fail to develop gastritis in response to H. felis infection. C57BL/6 mice do not, while BALB/c mice express, the PLA₂II enzyme. The H. felisinduced reduction in sPLA₂IB activity may weaken the gastric barrier by reducing the local concentration of arachidonic and linoleic acid, liberated from membrane phospholipids, the major precursors of cytoprotective prostaglandins. Data presented here suggest that both sPLA₂IB and sPLA₂II enzymes may contribute to the gastric response to Helicobacter infection.