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Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Konya, V; Philipose, S; Bálint, Z; Olschewski, A; Marsche, G; Sturm, EM; Schicho, R; Peskar, BA; Schuligoi, R; Heinemann, A.
Interaction of eosinophils with endothelial cells is modulated by prostaglandin EP4 receptors.
Eur J Immunol. 2011; 41(8):2379-2389
Doi: 10.1002/eji.201141460
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- Führende Autor*innen der Med Uni Graz
- Heinemann Akos
- Konya Viktoria
- Co-Autor*innen der Med Uni Graz
- Balint Zoltan
- Böhm Eva
- Marsche Gunther
- Olschewski Andrea
- Schicho Rudolf
- Schuligoi Rufina
- Sonia Philipose Sonia Philipose
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- Abstract:
- Eosinophil extravasation across the endothelium is a key feature of allergic inflammation. Here, we investigated the role of PGE(2) and its receptor, E-type prostanoid receptor (EP)-4, in the regulation of eosinophil interaction with human pulmonary microvascular endothelial cells. PGE(2) and the EP4 receptor agonist ONO AE1-329 significantly reduced eotaxin-induced eosinophil adhesion to fibronectin, and formation of filamentous actin and gelsolin-rich adhesive structures. These inhibitory effects were reversed by a selective EP4 receptor antagonist, ONO AE3-208. PGE(2) and the EP4 agonist prevented the activation and cell-surface clustering of β2 integrins, and L-selectin shedding of eosinophils. Under physiological flow conditions, eosinophils that were treated with the EP4 agonist showed reduced adhesion to endothelial monolayers upon stimulation with eotaxin, as well as after TNF-α-induced activation of the endothelial cells. Selective activation of EP1, EP2, and EP3 receptors did not alter eosinophil adhesion to endothelial cells, whereas the EP4 antagonist prevented PGE(2) from decreasing eosinophil adhesion. Finally, eosinophil transmigration across thrombin- and TNF-α-activated endothelial cells was effectively reduced by the EP4 agonist. These data suggest that PGE(2) -EP4 signaling might be protective against allergic responses by inhibiting the interaction of eosinophils with the endothelium and might hence be a useful therapeutic option for controlling inappropriate eosinophil infiltration.
- Find related publications in this database (using NLM MeSH Indexing)
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- Cell Line -
- Cell Movement - drug effects
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- Chemokine CCL11 - pharmacology
- Cyclopentanes - pharmacology
- Dinoprostone - pharmacology
- Endothelial Cells - cytology
- Eosinophils - cytology
- Fibronectins - metabolism
- Flow Cytometry -
- Gelsolin - metabolism
- Humans -
- L-Selectin - metabolism
- Methyl Ethers -
- Microscopy, Confocal -
- Naphthalenes - pharmacology
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- Receptors, Prostaglandin E, EP1 Subtype - metabolism
- Receptors, Prostaglandin E, EP2 Subtype - metabolism
- Receptors, Prostaglandin E, EP3 Subtype - metabolism
- Receptors, Prostaglandin E, EP4 Subtype - agonists
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- Find related publications in this database (Keywords)
- Adhesion
- Endothelium
- Eosinophils
- Migration
- Prostaglandins