Abstract：
:Mice rendered adenosine deaminase-deficient manifest an 'asthma' phenotype in the lungs that includes mast cell degranulation, eosinophilia, mucus hypersecretion and bronchial hyperresponsiveness. These changes can be reversed by enzyme therapy with adenosine deaminase, and attenuated by theophylline. Theophylline also blocks the pro-inflammatory effects of adenosine in allergen-challenged mice. Adenosine A(2A) receptors are an essential part of the physiological negative feedback mechanism for limitation and termination of both tissue-specific and systemic inflammatory responses. In recent clinical studies, increases in plasma adenosine have been shown to accompany exercise-induced asthma, and adenosine concentrations in exhaled breath condensate are increased in asthmatics. These new data provide support for a key role for adenosine in asthma, which has become increasingly persuasive in recent years. The evidence is now convincing, and the time has come for the asthma community to give its full support to the design and evaluation of molecules that mimic or block the biological effects of adenosine as potential novel therapeutics for this condition.
journal_name
Curr Opin Pharmacoljournal_title
Current opinion in pharmacologyauthors
Fozard JRdoi
10.1016/s1471-4892(03)00039-0keywords:
subject
Has Abstractpub_date
2003-06-01 00:00:00pages
264-9issue
3eissn
1471-4892issn
1471-4973pii
S1471489203000390journal_volume
3pub_type
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journal_title：Current opinion in pharmacology
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journal_title：Current opinion in pharmacology
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journal_title：Current opinion in pharmacology
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journal_title：Current opinion in pharmacology
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journal_title：Current opinion in pharmacology
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