Effect of bacterial endotoxin on the in vitro release of type II phospholipase-A2 and prostaglandin E2 from human placenta

The aim of this study was to establish the effect of bacterial endotoxin lipopolysaccharide (LPS) on the release of Type II phospholipase-A(2) (PLA(2)) and prostaglandin E-2 (PCE2) from late-pregnant human placental tissue incubated in vitro. Under basal conditions, immunoreactive Type II PLA(2) and PGE(2) were released from tissue explants in a time-dependent manner (up to 24 h, ANOVA, P<0.0001, n=6). The release of these mediators was not associated with a loss of cell membrane integrity, as indicated by concentrations of the intracellular enzyme, lactate dehydrogenase (LDH), in the incubation medium. Incubation of explants in the presence of LPS (0.001-100 mu g LPS/ml) significantly decreased PLA(2) tissue content (P<0.02, n=6) and increased the accumulation of PLA(2) and PGE(2) in the incubation medium (P<0.0001, n=6). The data obtained in this study indicated that Type II PLA(2) and PGE(2) are released from term placenta under basal conditions and that LPS stimulated their release. The associated decrease in PLA(2) tissue content is consistent with the hypothesis that LPS induces the release of stored PLA(2). This study identifies one pathway by which products of bacterial infection may induce the release of a pro-inflammatory, extracellularly active PLA(2) from intrauterine tissues that may promote the formation of phospholipid metabolites involved in the process of labour and delivery (e.g. the prostaglandins).