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Effect of an inhaled adenosine A 2A agonist on the allergen‐induced late asthmatic response
Author(s) -
Luijk B.,
Van Den Berge M.,
Kerstjens H. A. M.,
Postma D. S.,
Cass L.,
Sabin A.,
Lammers J.W. J.
Publication year - 2008
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/j.1398-9995.2007.01557.x
Subject(s) - medicine , agonist , fluticasone propionate , eosinophil cationic protein , inhalation , adenosine , asthma , allergen , eosinophil , adenosine receptor , immunology , pharmacology , receptor , allergy , anesthesia
Background: Adenosine receptor activation is suggested to play a role in asthmatic airway inflammation. Inhibition of adenosine receptors may have an effect on the late asthmatic response (LAR) after allergen inhalation and this mechanism could offer a potential new treatment in asthma. Methods: We evaluated the effect of an inhaled adenosine‐ 2A (A 2A )‐receptor agonist (GW328267X), 25 μg, in 15 nonsmoking atopic asthmatics who underwent an inhaled allergen challenge following twice daily treatment for 1 week in a double‐blind, placebo‐ and fluticasone propionate (250 μg) controlled study. Results: In contrast to fluticasone, treatment with the A 2A ‐receptor agonist neither significantly protect against the allergen‐induced early and late asthmatic reaction, nor the accompanying inflammatory response as measured by sputum total cell counts, number of EG2+ cells, and the concentration of interleukin‐8 and eosinophil cationic protein. Conclusion: The inhaled A 2A ‐receptor agonist, GW328267X, 25 μg does not affect the allergen‐induced LAR or the associated inflammatory response in asthma.