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Adenosine A 3 receptor stimulation inhibits migration of human eosinophils
Author(s) -
Knight Darryl,
Zheng Xueyan,
Rocchini Corinne,
Jacobson Marlene,
Bai Tony,
Walker Blair
Publication year - 1997
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.62.4.465
Subject(s) - chemotaxis , leukotriene b4 , stimulation , eosinophil , biology , adenosine , receptor , platelet activating factor , microbiology and biotechnology , inflammation , immunology , medicine , endocrinology , biochemistry , asthma
Activation of adenosine A 3 receptors (A 3 ‐R) produced a dose‐dependent reduction in the chemotaxis of human eosinophils to platelet‐activating factor (PAF), RANTES, and leukotriene B 4 (LTB 4 ) to a maximum of 58,48, and 52%, respectively ( P < 0.02). This effect was completely reversed by selective A 3 ‐R antagonists. In contrast, activation of A 1 or A 2a ‐R did not affect PAF‐induced eosinophil chemotaxis. PAF upregulated the expression of CD11b/CD18, down‐regulated L‐selectin, and also increased F‐actin assembly in eosinophils. The expression of these activation markers was not influenced by A 3 ‐R, A2a, or A 1 ‐R stimulation. Activation of A 3 ‐R may play an important role in inflammation by inhibiting eosinophil migration. J. Leukoc. Biol. 62: 465–468; 1997.