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Am J Physiol Lung Cell Mol Physiol (June 10, 2002). doi:10.1152/ajplung.00063.2002
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Articles in PresS, published online ahead of print June 10, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00063.2002
Submitted on February 19, 2002
Accepted on June 5, 2002

IN VITRO SENSITIZATION OF HUMAN BRONCHUS BY ß2-ADRENERGIC AGONISTS

CHRISTOPHE FAISY1, EMMANUEL NALINE2, JEAN-LUC DIEHL3, XAVIER EMONDS-ALT4, THIERRY CHINET2, and CHARLES ADVENIER2*

1 UPRES EA220, Laboratoire de Pharmacologie, 45 rue des Saint-Peres, 75006 Paris, Faculte de Medecine Paris-Ouest, UFR Biomedicale des Saint-Peres, Paris, France, Metropolitan; Service de Reanimation Medicale, 45 rue Leblanc 75908 Paris Cedex 15, Hopital Europeen Georges Pompidou, Paris, France, Metropolitan
2 UPRES EA220, Laboratoire de Pharmacologie, 45 rue des Saint-Peres, 75006 Paris, Faculte de Medecine Paris-Ouest, UFR Biomedicale des Saint-Peres, Paris, France, Metropolitan
3 Service de Reanimation Medicale, 45 rue Leblanc 75908 Paris Cedex 15, Hopital Europeen Georges Pompidou, Paris, France, Metropolitan
4 Sanofi Synthelabo Recherche, 371 Avenue du Pr Blayac, 34000 Montpellier, Montpellier, France, Metropolitan

* To whom correspondence should be addressed. E-mail: charles.advenier{at}wanadoo.fr.

Incubation of human distal bronchi from 48 patients with fenoterol (107 M, 15 h) induced sensitization characterized by an increase in maximal contraction to endothelin-1 (ET-1) and acetylcholine (ACh). Incubation of human bronchi with forskolin (10-6, 3.10-6 and 10-5 M), an adenylcyclase activator, reproduced sensitization to ET-1 and ACh. The sensitizing effect of fenoterol was inhibited by co-incubation with gliotoxin, an NF{kappa}B inhibitor, with dexamethasone, with indomethacin, a cyclo-oxygenase inhibitor, with GR 32191, a TP prostanoid receptor antagonist, with MK 476, a Cyst-LT1 leukotriene receptor antagonist, with SR 140333 + SR 48968 + SR 142801 (NK1, 2, 3 tachykinin receptor antagonists) ±HOE 140 (a bradykinin B2 receptor antagonist), with SB 203580, an inhibitor of the 38-kDa mitogen-activated protein kinase (p38MAPK) or with calphostin C, a protein kinase C (PKC) blocker. Our results suggest that chronic exposure to fenoterol involves proinflammatory effects mediated by NF{kappa}B and pathways implying leukotrienes, prostanoids, bradykinin, tachykinins, PKC and p38MAPK leading to the regulation of smooth muscle contraction to ET-1 and ACh.




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