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Am J Physiol Lung Cell Mol Physiol 285: L393-L404, 2003. First published May 2, 2003; doi:10.1152/ajplung.00030.2003
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{beta}-Adrenergic agonists inhibit corticosteroid-induced apoptosis of airway epithelial cells

Roberta Tse,1 Bertha A. Marroquin,1 Delbert R. Dorscheid,2 and Steven R. White1

1Section of Pulmonary and Critical Care Medicine, Division of Biological Sciences, University of Chicago, Chicago, Illinois 60637; and 2McDonald Research Laboratories and iCAPTURE Centre, University of British Columbia, Vancouver, British Columbia, Canada V6Z 1Y6

Submitted 30 January 2003 ; accepted in final form 22 April 2003

Airway epithelial damage is a feature of persistent asthma. Treatment with inhaled and oral corticosteroids may suppress inflammation and gain clinical control despite continued epithelial damage. We have previously demonstrated that corticosteroids elicit apoptosis of airway epithelial cells in culture. {beta}-Adrenergic receptor agonists are commonly used in asthma therapy and can inhibit corticosteroid-induced apoptosis of eosinophils. We tested the hypothesis that {beta}-adrenergic agonists would inhibit corticosteroid-induced airway epithelial cell apoptosis in cultured primary airway epithelial cells and in the cell line 1HAEo-. Albuterol treatment inhibited dexamethasone-induced apoptosis completely but did not inhibit apoptosis induced by Fas receptor activation. The protective effect of albuterol was duplicated by two different analogs of protein kinase A. The protective effect was not associated with increased translocation of the glucocorticoid receptor to the nucleus nor with changes in glucocorticoid receptor-mediated transcriptional activation or repression. We demonstrate that {beta}-adrenergic agonists can inhibit corticosteroid-induced apoptosis but not apoptosis induced by Fas activation. These data suggest that one potential deleterious effect of corticosteroid therapy in asthma can be prevented by concomitant {beta}-adrenergic agonist treatment.

airway epithelium; {beta}-adrenergic receptor agonist; protein kinase A


Address for reprint requests and other correspondence: S. R. White, Univ. of Chicago, Section of Pulmonary and Critical Care Medicine, 5841 S. Maryland Ave., MC 6076, Chicago, IL 60637 (E-mail: swhite{at}medicine.bsd.uchicago.edu).




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Y. Tesfaigzi
Roles of Apoptosis in Airway Epithelia
Am. J. Respir. Cell Mol. Biol., May 1, 2006; 34(5): 537 - 547.
[Abstract] [Full Text] [PDF]


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