| Abstrakt: |
The murine gastric mucosa possesses very high secretory type phospholipase A2 activity. Northern and Western blots indicated that the pancreatic type, sPLA2 IB represents the predominant form of sPLA2 enzymes present in the gastric mucosa. Both sPLA2 IB 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 sPLA2 IB 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 sPLA2 IB 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 PLA2 II enzyme. The H. felis induced reduction in sPLA2 IB 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 sPLA2 IB and sPLA2 II enzymes may contribute to the gastric response to Helicobacter infection. [ABSTRACT FROM AUTHOR] |
Full text from SpringerLink