• Agne Babusyte, Kristina Stravinskaite, Jolanta Jeroch, Jan Lötvall, Raimundas Sakalauskas, and Brigita Sitkauskiene.
• Laboratory of Pulmonology, Institute for Biomedical Research, Kaunas University of Medicine, Eiveniu 4, LT-50009, Kaunas, Lithuania. agne.babusyte@gmail.com
• Resp Res. 2007 Nov 14; 8: 81.

BackgroundSmoking 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.Methods39 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.ResultsThe 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 x 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 x 106/ml respectively, p < 0.05).ConclusionThe 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.

29 keywords...

hide…