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. Therefore, eosinophils are currently considered a major therapeutic target in allergic diseases. Prostaglandin (PG) E2 exerts anti-inflammatory and broncho-protective 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 [1].
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
The chemotaxis of human eosinophils towards the chemoattractant eotaxin was attenuated by PGE2 and the selective EP4 agonist ONO-AE1-329 in a concentrationdependent manner
Pretreatment of eosinophils with the adenylyl cyclase inhibitor SQ-22536, the protein kinase A inhibitor H-89 or the p38 MAP kinase inhibitor SB202190 did not prevent the inhibitory effect of PGE2, while the phosphatidyl inositol 3-kinase (PI3K) inhibitor LY-294002, triciribine, a specific inhibitor of Akt phosphorylation, and a myristoylated pseudosubstrate of protein kinase (PK) C-ζ, partially or completely reversed the inhibitory effect of PGE2 and ONO-AE1-329 on the migration of eosinophils towards eotaxin
Summary
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. Address: Institute of Experimental and Clinical Pharmacology, Medical University of Graz, 8010 Graz, Austria Email: Ákos Heinemann* - akos.heinemann@medunigraz.at * Corresponding author from 15th Scientific Symposium of the Austrian Pharmacological Society (APHAR) Joint meeting with the Hungarian Society of Experimental and Clinical Pharmacology (MFT) and the Slovenian Pharmacological Society (SDF) Graz, Austria.
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