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Upregulation of basic fibroblast growth factor in smokers with chronic bronchitis

F. Guddo¹, A. M. Vignola, ², M. Saetta³, S. Baraldo³, L. Siena², E. Balestro³, R. Zuin³, A. Papi⁴, P. Maestrelli⁵, L. M. Fabbri⁶, G. Bonsignore² and G. Turato³

¹ Pathology Unit, V. Cervello Hospital, and ² Institute of Lung Pathophysiology, National Research Council, Palermo, ³ Dept of Cardiothoracic and Vascular Sciences, Section of Respiratory Diseases, and ⁵ Dept of Environmental Medicine and Public Health, University of Padova, Padova, ⁴ Dept of Clinical and Experimental Medicine, Section of Respiratory Diseases, University of Ferrara, Ferrara, ⁶ Dept of Oncology and Hematology, Section of Respiratory Diseases, University of Modena and Reggio Emilia, Modena, Italy.

CORRESPONDENCE: M. Saetta, Divisione di Pneumologia, Dipartimento di Scienze Cardiologiche, Toraciche e Vascolari, Università degli Studi di Padova, Via Giustiniani 3, 35128 Padova, Italy. Fax: 39 0498213701. E-mail: marina.saetta{at}unipd.it

Keywords: Airway remodelling, cigarette smoking, chronic obstructive pulmonary disease, fibroblast growth factor receptor-1

Received: May 16, 2005
Accepted January 30, 2006

The aim of the study was to investigate the expression of basic fibroblast growth factor (bFGF) and its receptor, fibroblast growth factor receptor (FGFR)-1, in the central airways of smokers with chronic bronchitis.

The lobar bronchi from 17 subjects undergoing thoracotomy for solitary nodules were examined. All had a history of cigarette smoking, nine had symptoms of chronic bronchitis and airflow limitation, and eight were asymptomatic with normal lung function. Using immunohistochemical methods, bFGF and FGFR-1 expression in the total airway wall and the different airway compartments, i.e. bronchial glands, submucosal vessels and smooth muscle, was quantified. Moreover, to investigate the role of bFGF in angiogenesis, the number of submucosal vessels was quantified.

Smokers with chronic bronchitis had an increased bFGF expression in the total airway wall compared with asymptomatic smokers, which was mainly due to bFGF upregulation in bronchial glands. By contrast, the expression of FGFR-1 and the number of submucosal vessels was similar in the two groups of subjects examined.

In conclusion, smokers with chronic bronchitis have an increased expression of basic fibroblast growth factor in the central airways, which is mainly due to an increased expression in bronchial glands, suggesting the involvement of this growth factor in the pathogenesis of chronic bronchitis.

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