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Am J Physiol Lung Cell Mol Physiol 283: L1033-L1042, 2002. First published June 10, 2002; doi:10.1152/ajplung.00063.2002
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Vol. 283, Issue 5, L1033-L1042, November 2002

In vitro sensitization of human bronchus by beta 2-adrenergic agonists

Christophe Faisy1,2, Emmanuel Naline1, Jean-Luc Diehl2, Xavier Emonds-Alt3, Thierry Chinet1, and Charles Advenier1

1 Unité Propre de Recherche de l'Enseignement Supérior Equipe d'Accueil 220, Faculté de Médecine Paris-Ouest, Unité de Formation et de Recherche Biomédicale des Saint-Pères, 75006 Paris; 2 Service de Réanimation Médicale, Hôpital Européen Georges Pompidou, 75908 Paris Cedex 15; and 3 Sanofi Synthelabo Recherche, 34000 Montpellier, France

Incubation of human distal bronchi from 48 patients for 15 h with 10-7 M fenoterol induced sensitization characterized by an increase in maximal contraction to endothelin-1 (ET-1) and acetylcholine (ACh). Incubation of human bronchi with 10-6, 3 × 10-6, and 10-5 M forskolin (an adenyl cyclase activator) reproduced sensitization to ET-1 and ACh. The sensitizing effect of fenoterol was inhibited by coincubation with gliotoxine (a nuclear factor-kappa B inhibitor), dexamethasone, indomethacin (a cyclooxygenase inhibitor), GR-32191 (a TP prostanoid receptor antagonist), MK-476 (a cysteinyl leukotriene type 1 receptor antagonist), SR-140333 + SR-48968 + SR-142801 (neurokinin types 1, 2, and 3 tachykinin receptor antagonists) with or without HOE-140 (a bradykinin B2 receptor antagonist), SB-203580 (an inhibitor of the 38-kDa mitogen-activated protein kinase, p38MAPK), or calphostin C (a protein kinase C blocker). Our results suggest that chronic exposure to fenoterol induces proinflammatory effects mediated by nuclear factor-kappa B and pathways involving leukotrienes, prostanoids, bradykinin, tachykinins, protein kinase C, and p38MAPK, leading to the regulation of smooth muscle contraction to ET-1 and ACh.

beta 2-agonists; airway sensitization; airway smooth muscle; endothelin-1; asthma


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