Prostaglandin E-1 is able to increase migration of leukocytes through endothelial cell monolayers

Leukocyte interactions with endothelial cells play an important role during inflammatory processes. Leukocytes pass a monolayer of endothelial cells ( ECM) to migrate into the extravascular space. The aim of the current study was to investigate whether prostaglandin E-1 (PGE(1)) influences the proces s of leukocyte migration. In a prospective controlled study, the influence of prostaglandin E-1 (50-5000 ng/mL) on leukocyte migration through endothe lial cell monolayers (n = 7) was investigated. Human umbilical endothelial cells (HUVEC) and/or leukocytes were preincubated with clinically relevant, higher, and lower concentrations of prostaglandin E-1 and the amount of le ukocyte migration after 3 h was measured. HUVEC were cultured on microporou s membrane filters until achievement of a monolayer for investigation of le ukocyte migration. Polymorphonuclear leukocytes (PMNL) were isolated from h ealthy volunteers and PMNL migration was studied under the influence of PGE (1). In clinically relevant concentrations, PGE(1) was able to increase sig nificantly leukocyte migration through endothelial cell monolayers (205 +/- 7.8%, P < 0.05 compared to control; when treating PMNL alone, migration ra te was 120 +/- 9.2% compared to control, ns; only endothelial cell monolaye rs treated up to 145 +/- 10.2%, P < 0.05 compared to control) showing a dos e-dependent effect. In this assay, both cell types (PMNL and ECM) could be treated simultaneously, simulating the clinical situation after an iv admin istration. In conclusion, PGE(1) is able to increase leukocyte migration th rough endothelial cell monolayers when both cell types are pretreated. The treatment of either leukocytes or endothelial cell monolayers in the cell c oculture showed no significant increase. These findings support the theory that prostaglandins may play a major role during inflammation. Future clini cal studies are warranted to confirm this hypothesis. (C) Academic Press.