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pubmed:abstractText |
Mast cells are central to the development of bronchial inflammation and thus to bronchial hyperreactivity, the cardinal feature of asthma. Inflammation is due to the concerted action of mast cell-dependent vasoactive/spasmogenic mediators, chemotactic factors, and enzymes. Adenosine, a newly synthesized mast cell mediator (from adenosine triphosphate), is one of the important inflammatory mediators capable of causing bronchospasm and, by interacting with mast cell membrane receptors, of augmenting mediator release induced by antigen. These inflammatory and pro-asthmatic actions of adenosine can be inhibited by concentrations of theophylline achievable in humans that are insufficient to alter cyclic adenosine monophosphate metabolism. Thus, a new therapeutic consideration in the use of xanthine drugs is their ability to inhibit adenosine binding to cell surface receptors and thereby inhibit the effects of this purine nucleoside.
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