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 Blood, 24 September 2009, Vol. 114, No. 13, pp. 2774-2782.
Prepublished online as a Blood First Edition Paper on July 29, 2009; DOI 10.1182/blood-2009-05-220681.

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PHAGOCYTES, GRANULOCYTES, AND MYELOPOIESIS

Eosinophil viability is increased by acidic pH in a cAMP- and GPR65-dependent manner

Leah C. Kottyan1,2, Ann R. Collier1, Khanh H. Cao1, Kathryn A. Niese1, Megan Hedgebeth1, Caius G. Radu3,4, Owen N. Witte5,6, Gurjit K. Khurana Hershey1,2, Marc E. Rothenberg1,2, and Nives Zimmermann1,2

1 Cincinnati Children's Hospital Medical Center, OH; 2 Immunobiology Graduate Program, University of Cincinnati College of Medicine, OH; and 3 Crump Institute for Molecular Imaging, 4 Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, 5 Department of Microbiology, Immunology, and Molecular Genetics, and 6 Howard Hughes Medical Institute, University of California, Los Angeles

The microenvironment of the lung in asthma is acidic, yet the effect of acidity on inflammatory cells has not been well established. We now demonstrate that acidity inhibits eosinophil apoptosis and increases cellular viability in a dose-dependent manner between pH 7.5 and 6.0. Notably, acidity induced eosinophil cyclic adenosine 5'-monophosphate (cAMP) production and enhanced cellular viability in an adenylate cyclase–dependent manner. Furthermore, we identify G protein-coupled receptor 65 (GPR65) as the chief acid-sensing receptor expressed by eosinophils, as GPR65-deficient eosinophils were resistant to acid-induced eosinophil cAMP production and enhanced viability. Notably, GPR65–/– mice had attenuated airway eosinophilia and increased apoptosis in 2 distinct models of allergic airway disease. We conclude that eosinophil viability is increased in acidic microenvironments in a cAMP- and GPR65-dependent manner.


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