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Konya, V; Sturm, EM; Schratl, P; Beubler, E; Marsche, G; Schuligoi, R; Lippe, IT; Peskar, BA; Heinemann, A.
Endothelium-derived prostaglandin I(2) controls the migration of eosinophils.
J Allergy Clin Immunol. 2010; 125(5): 1105-1113. Doi: 10.1016/j.jaci.2009.12.002
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Führende Autor*innen der Med Uni Graz
Heinemann Akos
Konya Viktoria
Co-Autor*innen der Med Uni Graz
Beubler Eckhard
Böhm Eva
Lippe Irmgard Theresia
Luschnig Petra
Marsche Gunther
Peskar Bernhard
Schuligoi Rufina
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Abstract:
Background: Enhanced eosinophil migration from the blood into the tissue is a hallmark of allergic diseases. Prostaglandin (PG) I-2 is the major prostanoid released by endothelial cells. Mice deficient in PGI(2) receptors (IPs) show exaggerated eosinophilic inflammation in response to allergen. Objective: We set out to determine the role of PGI(2) in eosinophil trafficking. Methods: Human lung microvascular endothelial cells and purified human eosinophils were used to study adhesion and transendothelial migration. Morphologic studies were performed with fluorescence microscopy. Results: PGI(2) markedly attenuated the migration of eosinophils through cell-free filters but had no effect on neutrophil migration. The inhibitory effect of PGI(2) on eosinophils was prevented by the IP antagonist Cay10441 and the adenylyl cyclase inhibitor SQ22536. Similarly, PGI(2) prevented the adhesion of eosinophils to fibronectin and the rapid upregulation and activation of the adhesion molecule CD11b. IP expression on eosinophils was confirmed by means of flow cytometry and Western blotting. Furthermore, when endothelial cells were treated with the COX inhibitor diclofenac to abolish PGI(2) production, adhesion of eosinophils to endothelial monolayers and subsequent transendothelial migration were markedly enhanced. Similarly, the IP antagonist enhanced eosinophil adhesion to endothelial cells. Inhibition of PGI(2) biosynthesis decreased the electrical resistance of endothelial monolayers and compromised the texture of adherent junctions, as visualized by means of VE-cadherin and F-actin staining. Conclusion: We propose that endothelium-derived PGI(2) might be fundamental for the maintenance of the endothelial barrier function against infiltrating cells. These results suggest that selective IP agonists might have beneficial effects in allergic inflammation. (J Allergy Clin Immunol 2010;125:1105-13.)
Find related publications in this database (using NLM MeSH Indexing)
Cell Adhesion - drug effects
Cells, Cultured -
Chemotaxis, Leukocyte - drug effects
Endothelial Cells - cytology
Endothelium, Vascular - cytology
Eosinophils - drug effects
Epoprostenol - metabolism
Humans -
Lung - blood supply

Find related publications in this database (Keywords)
Endothelial cells
eosinophils
COX
prostaglandins
migration
adhesion
allergy
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