Premium
Inhibition of eotaxin‐mediated human eosinophil activation and migration by the selective cyclic nucleotide phosphodiesterase type 4 inhibitor rolipram
Author(s) -
Santamaria Luis F,
Maria Palacios Jose,
Beleta Jorge
Publication year - 1997
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0701243
Subject(s) - rolipram , eotaxin , eosinophil , phosphodiesterase , chemotaxis , chemistry , zaprinast , phosphodiesterase inhibitor , flow cytometry , immunology , pharmacology , microbiology and biotechnology , biochemistry , biology , enzyme , receptor , asthma
The effect of the selective type 4 phosphodiesterase (PDE 4) inhibitor rolipram on human eosinophil activation and migration mediated by eotaxin was investigated. Studies were performed with human freshly isolated eosinophils from peripheral blood of healthy donors by a magnetic cell separation (MACS) technique to a purity>99%. To test the effect of rolipram, eosinophils were stimulated with recombinant human eotaxin and the cell surface activation markers CD11b and L‐selectin were analysed by flow cytometry. Furthermore, eotaxin mediated eosinophil migration was measured in a transendothelial chemotaxis assay. Our results indicate that rolipram inhibited eotaxin‐induced CD11b up‐regulation up to 60.6±7.6% at the highest tested dose (10μ m ), whereas transendothelial chemotaxis was partially inhibited reaching a plateau of approx. 30% at a rolipram concentration of 0.1μ m . We conclude that the selective PDE 4 inhibitor rolipram decreases eotaxin mediated eosinophil activation, an observation that may contribute to elucidate the mechanism by which PDE 4 inhibitors reduce antigen‐induced eosinophil infiltration in different animal models of allergic inflammation.