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Results Under basal conditions, the major prostaglandin released by human microvascular endothelial cells is PGI2. Exogenous PGI2 markedly attenuated the migration of isolated eosinophils through cell-free filters. This effect was prevented by the IP receptor antagonist Cay10441 and the adenylyl cyclase inhibitor SQ29548. Treatment of endothelial cells with diclofenac, a non-selective COX inhibitor, abolished the PGI2 production which was accompanied by enhanced eosinophil adhesion to endothelial monolayers. Similarly, the transmigration of eosinophils through endothelial monolayers was enhanced by diclofenac. The diclofenac treatment itself decreased the electrical resistance of endothelial monolayers and compromised the intercellular cell junctions as visualized by VE-cadherin staining.

The role of prostacyclin in the interaction of endothelial cells and eosinophil granulocytes