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Impact of acute exposure to tobacco smoke on gelatinases in the bronchoalveolar space

¹ Lung Immunology Group, Dept of Internal Medicine/Respiratory Medicine and Allergology, Sahlgrenska Academy, University of Gothenburg, Göteborg, Sweden. ² Depts of Medicine, and ³ Pharmacology, Cooperative Research Centre for Chronic Inflammatory Disease, University of Melbourne, Melbourne, Australia.

CORRESPONDENCE: P. Glader, Lung Immunology Group, University of Gothenburg, Guldhedsgatan 10A, 413 46 Göteborg, Sweden. Fax: 46 31413290. E-mail: Pernilla.Glader{at}gu.se

Keywords: Chronic obstructive pulmonary disease, macrophage, matrix metalloproteinase 9, neutrophils, tissue inhibitor of matrix metalloproteinase

Received: September 14, 2007
Accepted March 26, 2008

Clinical studies have indicated increased gelatinase activity in the airways of patients suffering from chronic obstructive pulmonary disease caused by tobacco smoke. The present study aimed to determine whether acute exposure to tobacco smoke per se causes a substantial and lasting impact on gelatinases and their inhibitors in the peripheral airways of atopic and nonatopic human subjects.

Bronchoscopy with bronchoalveolar lavage (BAL) was performed on occasional smokers with and without atopy before and after smoking 10 cigarettes over a 48-h period. Samples from a group of never-smokers not exposed to tobacco smoke served as controls. Gelatinase identity and activity were measured using zymography, and gelatinase activity assay and concentrations of matrix metalloproteinase (MMP)-2, MMP-9, tissue inhibitor of MMP (TIMP)-1 and TIMP-2 were measured using ELISA.

The results revealed no pronounced changes in identity, net activity or concentration of the gelatinases or changes in concentrations of TIMP-1 and TIMP-2 in BAL fluid before and after acute exposure to tobacco smoke.

In conclusion, the present experimental study indicates that acute exposure to tobacco smoke does not cause any substantial impact on gelatinases or their inhibitors in the peripheral airways, irrespective of atopy status, a finding that is compatible with the fact that it takes many years of tobacco smoking to establish chronic obstructive pulmonary disease.