Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD

Agne Babusyte¹ , Kristina Stravinskaite² , Jolanta Jeroch¹ , Jan Lötvall³ , Raimundas Sakalauskas² and Brigita Sitkauskiene¹^,2

¹Laboratory of Pulmonology, Institute for Biomedical Research, Kaunas University of Medicine, Eiveniu 4, LT-50009, Kaunas, Lithuania

²Department of Pulmonology and Immunology, Kaunas University of Medicine, Eiveniu 2, LT-50009, Kaunas, Lithuania

³The Lung Pharmacology Group, Department of Respiratory Medicine and Allergology, Institute of Internal Medicine, Göteborg University, Guldhedsgatan 10A, 413 46 Gothenburg, Sweden

author email corresponding author email

Respiratory Research 2007, 8:81doi:10.1186/1465-9921-8-81


Published:	14 November 2007

Abstract

Background

Smoking activates and recruits inflammatory cells and proteases to the airways. Matrix metalloproteinase (MMP)-12 may be a key mediator in smoke induced emphysema. However, the influence of smoking and its cessation on airway inflammation and MMP-12 expression during COPD is still unknown. We aimed to analyse airway inflammatory cell patterns in induced sputum (IS) and bronchoalveolar lavage (BAL) from COPD patients who are active smokers and who have ceased smoking >2 years ago.

Methods

39 COPD outpatients – smokers (n = 22) and ex-smokers (n = 17) were studied. 8 'healthy' smokers and 11 healthy never-smokers were tested as the control groups. IS and BAL samples were obtained for differential and MMP-12⁺-macrophages count analysis.

Results

The number of IS neutrophils was higher in both COPD groups compared to both controls. The amount of BAL neutrophils was higher in COPD smokers compared to healthy never-smokers. The number of BAL MMP-12⁺-macrophages was higher in COPD smokers (1.6 ± 0.3 × 10⁶/ml) compared to COPD ex-smokers, 'healthy' smokers and healthy never-smokers (0.9 ± 0.4, 0.4 ± 0.2, 0.2 ± 0.1 × 10⁶/ml respectively, p < 0.05).

Conclusion

The lower amount of BAL neutrophils in COPD ex-smokers, compared to COPD smokers, suggests positive alterations in alveolar compartment after smoking cessation. Smoking and disease itself may stimulate MMP-12 expression in airway compartments (IS and BAL) from COPD patients.