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Am J Physiol Lung Cell Mol Physiol 283: L1072-L1078, 2002. First published June 21, 2002; doi:10.1152/ajplung.00076.2002
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Vol. 283, Issue 5, L1072-L1078, November 2002

An endothelin receptor antagonist, SB-217242, inhibits airway hyperresponsiveness in allergic mice

Peter J. Henry1,2, Tracy S. Mann1, Angela C. D'Aprile1, Glenn J. Self1, and Roy G. Goldie1,2

1 Department of Pharmacology, University of Western Australia, Crawley 6009; and 2 Western Australian Institute for Medical Research, Nedlands 6009, Australia

Within the airways, endothelin-1 (ET-1) can exert a range of prominent effects, including airway smooth muscle contraction, bronchial obstruction, airway wall edema, and airway remodeling. ET-1 also possesses proinflammatory properties and contributes to the late-phase response in allergic airways. However, there is no direct evidence for the contribution of endogenous ET-1 to airway hyperresponsiveness in allergic airways. Allergic inflammation induced in mice by sensitization and challenge with the house dust mite allergen Der P1 was associated with elevated levels of ET-1 within the lung, increased numbers of eosinophils within bronchoalveolar lavage fluid and tissue sections, and development of airway hyperresponsiveness to methacholine (P < 0.05, n = 6 mice per group). Treatment of allergic mice with an endothelin receptor antagonist, SB-217242 (30 mg · kg-1 · day-1), during allergen challenge markedly inhibited airway eosinophilia (bronchoalveolar lavage fluid and tissue) and development of airway hyperresponsiveness. These findings provide direct evidence for a mediator role for ET-1 in development of airway hyperresponsiveness and airway eosinophilia in Der P1-sensitized mice after antigen challenge.

eosinophils; allergic inflammation


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