Related Experiment Video
Updated: Jul 10, 2026

Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice
Published on: January 16, 2015
Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD
Agne Babusyte1, Kristina Stravinskaite, Jolanta Jeroch
1Laboratory of Pulmonology, Institute for Biomedical Research, Kaunas University of Medicine, Eiveniu 4, LT-50009, Kaunas, Lithuania. agne.babusyte@gmail.com
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 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).
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.
Related Concept Videos
Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features
Chronic Obstructive Pulmonary Disease-II: Pathophysiology
Chronic Inflammation
Chronic Obstructive Pulmonary Disease II: Emphysema
Chronic Obstructive Pulmonary Disease IV: Clinical Manifestations
Chronic Obstructive Pulmonary Disease I: Introduction
COPD: Pathogenesis and Clinical Features
The primary cause for the onset of COPD is cigarette smoking and exposure to air pollution. These hazardous factors initiate a chain reaction within the lungs, resulting in chronic inflammation, damage to the airways, and a...