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A1 antagonism in asthma: better than coffee?
Stephen L. Tilley, Richard C. Boucher
Stephen L. Tilley, Richard C. Boucher
Published January 3, 2005
Citation Information: J Clin Invest. 2005;115(1):13-16. https://doi.org/10.1172/JCI24009.
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Commentary

A1 antagonism in asthma: better than coffee?

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Abstract

Adenosine is a ubiquitous biological mediator with the capacity to produce both pro- and anti-inflammatory effects in tissues. Proinflammatory and bronchoconstrictive actions of adenosine in the asthmatic lung are well recognized, with the latter being mediated, in part, through A1 receptor activation on airway smooth muscle. In this issue of the JCI, Sun et al. report findings in adenosine deaminase–deficient mice that suggest the occurrence of anti-inflammatory actions of adenosine in the lung, mediated through A1 adenosine receptors on macrophages. Here we discuss the history of the study of adenosine receptor ligands for asthma and how enhanced understanding of adenosine receptor biology may aid in the rational exploitation of these receptors as therapeutic targets.

Authors

Stephen L. Tilley, Richard C. Boucher

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Figure 1

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Extracellular adenosine is produced predominantly by the metabolism of A...
Extracellular adenosine is produced predominantly by the metabolism of ATP released from cells. ATP is sequentially dephosphorylated by a series of membrane-bound and soluble ectonucleotidases to produce adenosine. Adenosine can act at 4 different 7-transmembrane, G-protein–coupled receptors present on the surfaces of both infiltrating leukocytes and resident parenchymal cells. While both proinflammatory and anti-inflammatory signals can be sent depending on the specific adenosine receptor activated, adenosine produces a net proinflammatory effect in the asthmatic airway. ADA is the primary catabolic enzyme for adenosine, and its absence in ADA-deficient mice results in marked elevations of extracellular adenosine. Elevations of extracellular adenosine are present in the asthmatic lung due to both increased release of ATP from cells and inhibition of ADA by local hypoxia. E-NPPs, ectonucleotide pyrophosphatase/phospho-diesterases; AP, alkaline phosphatase; NTPDases, ectonucleoside triphosphate-diphosphohydrolases.

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