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Effect of an inhaled adenosine A₂A agonist on the allergen-induced late asthmatic response

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. We evaluated the effect...

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Bibliographic Details
Published in:Allergy (Copenhagen) 2008, Vol.63 (1), p.75-80
Main Authors: Luijk, B, van den Berge, M, Kerstjens, H.A.M, Postma, D.S, Cass, L, Sabin, A, Lammers, J.-W.J
Format: Article
Language:English
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Summary: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. We evaluated the effect of an inhaled adenosine-₂A (A₂A)-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. In contrast to fluticasone, treatment with the A₂A-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. The inhaled A₂A-receptor agonist, GW328267X, 25 μg does not affect the allergen-induced LAR or the associated inflammatory response in asthma.
ISSN:0105-4538
1398-9995
DOI:10.1111/j.1398-9995.2007.01557.x