A sub(3) Adenosine Receptor Signaling Contributes to Airway Inflammation and Mucus Production in Adenosine Deaminase-Deficient Mice

A sub(3) Adenosine Receptor Signaling Contributes to Airway Inflammation and Mucus Production in Adenosine Deaminase-Deficient Mice

Adenosine signaling has been implicated in chronic lung diseases such as asthma and chronic obstructive pulmonary disease; however, the specific roles of the various adenosine receptors in processes central to these disorders are not well understood. In this study, we have investigated the role(s) o...

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Bibliographic Details
Published in:The Journal of immunology (1950) Vol. 173; no. 2; pp. 1380 - 1389
Main Authors: Young, Hays WJ, Molina, Jose G, Dimina, Dawn, Zhong, Hongyan, Jacobson, Marlene, Chan, Lee-Nien L, Chan, Teh-Sheng, Lee, James J, Blackburn, Michael R
Format: Journal Article
Language:English
Published: 15-07-2004
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Summary:Adenosine signaling has been implicated in chronic lung diseases such as asthma and chronic obstructive pulmonary disease; however, the specific roles of the various adenosine receptors in processes central to these disorders are not well understood. In this study, we have investigated the role(s) of the A sub(3) adenosine receptor in adenosine-dependent pulmonary inflammation observed in adenosine deaminase (ADA)-deficient mice. The A sub(3) receptor (A sub(3)R) was found to be expressed in eosinophils and mucus-producing cells in the airways of ADA-deficient mice. Treatment of ADA-deficient mice with MRS 1523, a selective A sub(3)R antagonist, prevented airway eosinophilia and mucus production. Similar findings were seen in the lungs of ADA/A sub(3) double knockout mice. Although eosinophils were decreased in the airways of ADA-deficient mice following antagonism or removal of the A sub(3)R, elevations in circulating and lung interstitial eosinophils persisted, suggesting signaling through the A sub(3)R is needed for the migration of eosinophils into the airways. These findings identify an important role for the A sub(3)R in regulating lung eosinophilia and mucus production in an environment of elevated adenosine.
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ISSN:0022-1767