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* Department of Biochemistry and Molecular Biology, University of Texas-Houston Medical School, Houston, TX 77030;
Department of Biochemistry and Molecular Biology, Mayo Clinic, S. C. Johnson Medical Research Center, Scottsdale, AZ 85259;
Department of Neuroscience, Merck Research Laboratories, West Point, PA 19486; and Departments of
Human Biological Chemistry and
¶
Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555
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 A3 adenosine receptor in adenosine-dependent pulmonary inflammation observed in adenosine deaminase (ADA)-deficient mice. The A3 receptor (A3R) 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 A3R antagonist, prevented airway eosinophilia and mucus production. Similar findings were seen in the lungs of ADA/A3 double knockout mice. Although eosinophils were decreased in the airways of ADA-deficient mice following antagonism or removal of the A3R, elevations in circulating and lung interstitial eosinophils persisted, suggesting signaling through the A3R is needed for the migration of eosinophils into the airways. These findings identify an important role for the A3R in regulating lung eosinophilia and mucus production in an environment of elevated adenosine.
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