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Am J Physiol Lung Cell Mol Physiol 284: L133-L139, 2003. First published August 16, 2002; doi:10.1152/ajplung.00217.2002
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Vol. 284, Issue 1, L133-L139, January 2003

Beclomethasone rapidly ablates allergen-induced beta 2- adrenoceptor pathway dysfunction in human isolated bronchi

Lorenzo Brichetto, Manlio Milanese, Pingfang Song, Mauro Patrone, Emanuele Crimi, Kai Rehder, and Vito Brusasco

Dipartimenti di Scienze Motorie e Riabilitative, di Medicina Interna, e di Medicina Sperimentale, Università di Genova, 16132 Genoa, Italy

Bronchial rings from nonatopic humans were passively sensitized with serum from allergic subjects. Allergen challenge significantly reduced the relaxant effect of salbutamol on carbachol-induced contractions, suggesting beta 2-adrenoceptor (beta 2-AR) pathway dysfunction. Incubation of challenged rings for 3 h with 3 × 10-6 M beclomethasone dipropionate (BDP) restored the relaxant effect, suggesting reversal of beta 2-AR pathway dysfunction. Incubation with the Gsalpha protein-stimulating cholera toxin attenuated contractile responses to carbachol significantly less in challenged than in unchallenged rings. Treatment of challenged rings with BDP resulted in an inhibitory effect of cholera toxin that was similar to the effect in unchallenged rings. Gsalpha protein expression was not significantly altered by BDP, suggesting that the activity of Gsalpha protein was increased. Relaxation of challenged rings by forskolin was not significantly affected by BDP, suggesting that beta 2-AR pathway dysfunction was proximal to the adenylyl cyclase. In conclusion, short-term (3-h) treatment with BDP after allergen challenge ablated beta 2-AR pathway dysfunction by increasing the activity of the Gsalpha protein in human isolated bronchi.

asthma; cholera toxin; corticosteroids; Gsalpha protein; passive sensitization


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