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Vasoactive intestinal peptide receptors in the airways of smokers with chronic bronchitis

Depts of ¹ Clinical and Experimental Medicine, and ² Surgery, Anaesthesiology and Radiology, University of Ferrara, Ferrara, and ³ Dept of Respiratory Diseases, University of Modena and Reggio Emilia, Modena, Italy

CORRESPONDENCE: C.E. Mapp, Dipartimento diMedicina Clinica e Sperimentale, Sezione di Igiene e Medicina del Lavoro, via Fossato di Mortara 64/b, 44100 Ferrara, Italy. Fax: 39 0532205066. E-mail: map@unife.it

Keywords: Mucus secretion, neuropeptide receptors, vasoactive intestinal peptide

Received: March 15, 2004
Accepted August 12, 2004

This study was supported by Consorzio Ferrararicerche (Ferrara, Italy), MURST (Minister of University and Scientific Research, Rome, Italy), and ARCA (Associazione per la Ricerca e la Cura dell'Asma, Padova, Italy).

Vasoactive intestinal peptide (VIP) is a neuropeptide involved in the regulation of airway mucus secretion. The biological functions of VIP are mediated through two receptors, the vasoactive intestinal peptide receptor type 1 (VPAC1R) and type 2 (VPAC2R). The aim of this study was to quantify the expression of both VPAC1R and VPAC2R in the central airways of smokers with chronic bronchitis.

Surgical specimens were obtained from 33 smokers undergoing thoracotomy for localised pulmonary lesions: 23 smokers with symptoms of chronic bronchitis and 10 asymptomatic smokers with normal lung function.

By using immunohistochemical and microscopic analysis, an increased expression of VPAC1R, but not VPAC2R, was found in bronchial epithelium, bronchial glands and vessels of smokers with symptoms of chronic bronchitis compared with asymptomatic smokers. Smokers with symptoms of chronic bronchitis also had an increased number of mononuclear cells positive for both VPAC1R and VPAC2R in the bronchial submucosa.

In conclusion, the expression of type 1 and type 2 vasoactive intestinal peptide receptors is increased in the central airways of smokers with chronic bronchitis, suggesting their possible involvement in the pathogenesis of chronic bronchitis.