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Open AccessMeeting abstractThe role of prostacyclin in the interaction of endothelial cells and eosinophil granulocytesViktória Kónya1, Eva M Sturm1, Zoltán Bálint2, Martin Krenn3 and Ákos Heinemann*1

Address: 1Institute of Experimental and Clinical Pharmacology, Medical University of Graz, 8010 Graz, Austria, 2Department of Anaesthesiology, Medical University of Graz, 8036 Graz, Austria and 3Institute of Pharmacology and Toxicology, University of Graz, 8010 Graz, Austria

Email: Ákos Heinemann* - akos.heineman@meduni-graz.at

* Corresponding author

BackgroundEnhanced eosinophil migration from the blood into thetissue is a hallmark of bronchial asthma and other allergicdiseases. So far, very little is known how the function ofvascular endothelial cells is modulated in this process.Our aim was to characterize the role of prostacyclin(PGI2) in endothelial function and endothelium-eosi-nophil interaction.

Materials and methodsCell interaction studies, like adhesion and transmigrationassays, were performed with freshly isolated human bloodeosinophils on confluent layers of human lung microvas-cular endothelial cells. The changes in endothelial monol-ayer integrity were detected by means of transendothelialelectrical resistance and by fluorescence microscopy.

ResultsUnder basal conditions, the major prostaglandin releasedby human microvascular endothelial cells is PGI2. Exoge-nous PGI2 markedly attenuated the migration of isolatedeosinophils through cell-free filters. This effect was pre-vented by the IP receptor antagonist Cay10441 and theadenylyl cyclase inhibitor SQ29548. Treatment ofendothelial cells with diclofenac, a non-selective COXinhibitor, abolished the PGI2 production which wasaccompanied by enhanced eosinophil adhesion toendothelial monolayers. Similarly, the transmigration of

eosinophils through endothelial monolayers wasenhanced by diclofenac. The diclofenac treatment itselfdecreased the electrical resistance of endothelial monolay-ers and compromised the intercellular cell junctions asvisualized by VE-cadherin staining.

ConclusionBased on these observations, we conclude that the basalsynthesis of PGI2 by endothelial cells can down-regulatethe endothelial adhesion and transmigration of eosi-nophils. Furthermore, endogenous PGI2 seems to beimportant for the maintenance of endothelium barrierfunction. These results suggest that PGI2 may have a pro-tective role in the case of allergic inflammation and pro-vide a novel explanation for previous observations that IPknock-out mice show enhanced eosinophilic inflamma-tion in response to allergen [1].

References1. Takahashi Y, Tokuoka S, Masuda T, Hirano Y, Nagao M, Tanaka H,

Inagaki N, Narumiya S, Nagai H: Augmentation of allergic inflam-mation in prostanoid IP receptor deficient mice. Br J Pharma-col 2002, 137:315-322.

from 14th Scientific Symposium of the Austrian Pharmacological Society (APHAR)Innsbruck, Austria. 21–22 November 2008

Published: 5 November 2008

BMC Pharmacology 2008, 8(Suppl 1):A13 doi:10.1186/1471-2210-8-S1-A13

<supplement> <title> <p>14^thScientific Symposium of the Austrian Pharmacological Society (APHAR)</p> </title> <editor>Andrea Laslop and Thomas Griesbacher</editor> <note>Meeting abstracts – A single PDF containing all abstracts in this Supplement is available <a href="http://www.biomedcentral.com/content/files/pdf/1471-2210-8-S1-full.pdf">here</a>.</note> <url>http://www.biomedcentral.com/content/pdf/1471-2210-8-S1-info.pdf</url> </supplement>

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© 2008 Kónya et al; licensee BioMed Central Ltd.