title: Prostaglandin E(1) is able to increase migration of leukocytes through endothelial cell monolayers.
abstract: 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 process of leukocyte migration. In a prospective controlled study, the influence of prostaglandin E(1) (50-5000 ng/mL) on leukocyte migration through endothelial 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 leukocyte migration after 3 h was measured. HUVEC were cultured on microporous membrane filters until achievement of a monolayer for investigation of leukocyte migration. Polymorphonuclear leukocytes (PMNL) were isolated from healthy volunteers and PMNL migration was studied under the influence of PGE(1). In clinically relevant concentrations, PGE(1) was able to increase significantly leukocyte migration through endothelial cell monolayers (205 +/- 7.8%, P < 0.05 compared to control; when treating PMNL alone, migration rate was 120 +/- 9.2% compared to control, ns; only endothelial cell monolayers treated up to 145 +/- 10.2%, P < 0.05 compared to control) showing a dose-dependent effect. In this assay, both cell types (PMNL and ECM) could be treated simultaneously, simulating the clinical situation after an iv administration. In conclusion, PGE(1) is able to increase leukocyte migration through endothelial cell monolayers when both cell types are pretreated. The treatment of either leukocytes or endothelial cell monolayers in the cell coculture showed no significant increase. These findings support the theory that prostaglandins may play a major role during inflammation. Future clinical studies are warranted to confirm this hypothesis.
authors.affiliation: Department of Medical and Chemical Laboratory Diagnostics, University of Vienna, Vienna, Austria.
authors.forename: R
authors.initials: R
authors.lastname: Hofbauer
authors.forename: D
authors.initials: D
authors.lastname: Moser
authors.forename: A D
authors.initials: AD
authors.lastname: Kaye
authors.forename: S
authors.initials: S
authors.lastname: Knapp
authors.forename: B
authors.initials: B
authors.lastname: Gmeiner
authors.forename: S
authors.initials: S
authors.lastname: Kapiotis
authors.forename: O
authors.initials: O
authors.lastname: Wagner
authors.forename: M
authors.initials: M
authors.lastname: Frass
mesh_terms: D000328:Adult; D000527:Alprostadil / Q000494:pharmacology*; D002478:Cells, Cultured; D002634:Chemotaxis, Leukocyte / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000166:cytology*; D006801:Humans; D007249:Inflammation; D008855:Microscopy, Electron, Scanning; D014471:Umbilical Veins
chemical_list: D000527:Alprostadil