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This Article Full Text Full Text (PDF) All Versions of this Article: 293/1/L25    most recent 00058.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Hua, X. Articles by Tilley, S. L. Search for Related Content PubMed PubMed Citation Articles by Hua, X. Articles by Tilley, S. L.

EDITORIAL FOCUS

Involvement of A₁ adenosine receptors and neural pathways in adenosine-induced bronchoconstriction in mice

¹Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of North Carolina at Chapel Hill, Chapel Hill, and ²Department of Internal Medicine, Center for Human Genomics, Wake Forest University, Winston-Salem, North Carolina

Submitted 12 February 2007 ; accepted in final form 18 April 2007

High levels of adenosine can be measured from the lungs of asthmatics, and it is well recognized that aerosolized 5'AMP, the precursor of adenosine, elicits robust bronchoconstriction in patients with this disease. Characterization of mice with elevated adenosine levels secondary to the loss of adenosine deaminase (ADA) expression, the primary metabolic enzyme for adenosine, further support a role for this ubiquitous mediator in the pathogenesis of asthma. To begin to identify pathways by which adenosine can alter airway tone, we examined adenosine-induced bronchoconstriction in four mouse lines, each lacking one of the receptors for this nucleoside. We show, using direct measures of airway mechanics, that adenosine can increase airway resistance and that this increase in resistance is mediated by binding the A₁ receptor. Further examination of this response using pharmacologically, surgically, and genetically manipulated mice supports a model in which adenosine-induced bronchoconstriction occurs indirectly through the activation of sensory neurons.

knockout; mast cell; nerves

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