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ORIGINAL ARTICLE |
1 Lung Immunology Group, Dept of Internal Medicine/Respiratory Medicine & Allergology, Sahlgrenska Academy at Göteborg University, Sweden
2 Cooperative Research Centre for Chronic Inflammatory Disease, Depts of Medicine and Pharmacology, University of Melbourne, Australia
* To whom correspondence should be addressed. E-mail: Pernilla.Glader{at}gu.se.
| Abstract |
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Clinical studies have indicated an increased gelatinase activity in the airways of patients suffering from COPD caused by tobacco smoke. This 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 non-atopic human subjects.
Bronchoscopy with bronchoalveolar lavage 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 MMP-2, MMP-9, 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 in concentrations of TIMP-1 and TIMP-2 in bronchoalveolar lavage fluid before and after acute exposure to tobacco smoke. In conclusion, this experimental study indicates that acute exposure to tobacco smoke does not cause any substantial impact on gelatinases or their inhibitors in the peripheral airways, irrespectively of atopy status; a finding that is compatible with the fact that it takes many years of tobacco smoking to establish COPD.
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