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G_q Signaling Is Required for Allergen-Induced Pulmonary Eosinophilia¹

Michael T. Borchers^*, Paul J. Justice, Tracy Ansay, Valeria Mancino, Michael P. McGarry^*, Jeffrey Crosby, Melvin I. Simon, Nancy A. Lee and James J. Lee^2,*

Divisions of ^* Pulmonary Medicine and Hematology and Oncology, Mayo Clinic, Scottsdale AZ 85259; and Division of Biology, California Institute of Technology, Pasadena, CA 91125

The complexity and magnitude of interactions leading to the selective infiltration of eosinophils in response to inhaled allergens are formidable obstacles to a larger understanding of the pulmonary pathology associated with allergic asthma. This study uses knockout mice to demonstrate a novel function for the heterotrimeric G protein, G_q, in the regulation of pulmonary eosinophil recruitment. In the absence of G_q signaling, eosinophils failed to accumulate in the lungs following allergen challenge. These studies demonstrate that the inhibition of eosinophil accumulation in the airways is attributed to the failure of hemopoietically derived cells to elaborate GM-CSF in the airways. The data suggest that activation of a G_q-coupled receptor(s) on resident leukocytes in the lung elicits expression of GM-CSF, which, in turn, is required for allergen-induced pulmonary eosinophilia, identifying a novel pathway of eosinophil-associated effector functions leading to pulmonary pathology in diseases such as asthma.

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