Abstract
Background The accumulation of eosinophils in lung tissue is a hallmark of asthma, and it is believed that eosinophils play a crucial pathogenic role in allergic inflammation. Prostaglandin (PG) E2 exerts anti-inflammatory and bronchoprotective mechanisms in asthma, but the underlying mechanisms have remained unclear. We have shown previously that PGE2 and the EP2 receptor agonist butaprost inhibit eosinophil trafficking in vitro and in vivo.
Highlights
The accumulation of eosinophils in lung tissue is a hallmark of asthma, and it is believed that eosinophils play a crucial pathogenic role in allergic inflammation
We have shown previously that PGE2 and the EP2 receptor agonist butaprost inhibit eosinophil trafficking in vitro and in vivo
Tors revealed that the inhibitory effect of EP4 stimulation on eosinophil migration depended upon activation of phosphatidylinositol 3-kinase and protein kinase C, but not cAMP
Summary
Address: Institute of Experimental and Clinical Pharmacology, Medical University of Graz, 8010 Graz, Austria. Published: 12 November 2009 BMC Pharmacology 2009, 9(Suppl 2):A2 doi:10.1186/1471-2210-9-S2-A2. 15th Scientific Symposium of the Austrian Pharmacological Society (APHAR) Andrea Laslop and Thomas Griesbacher Meeting abstracts - A single PDF containing all abstracts in this Supplement is available here. http://www.biomedcentral.com/content/pdf/1471-2210-9-S2-info.pdf
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