Summary
Introduction: Cigarette smoking is a major risk factor for chronic obstructive pulmonary disease (COPD). Exposure to cigarette smoke may stimulate inflammatory response and activate polymorphonuclear leukocytes (PMN) thus resulting in secretion of cellular proteases. The aim of our study was to explore the effect of cigarette smoke extract (CSE) on the release of matrix metalloproteinase-9 (MMP-9) from PMN.
Methods: The study included 23 patients with stable COPD and 9 healthy controls. PMN were isolated from blood of all participants and exposed to 4% CSE or basal culture medium (0% CSE) for 20 h. MMP-9 concentration in PMN culture media was measured using the ELISA method.
Results: Exposure of PMN to 4% CSE did not cause cytotoxic effects, as determined by no changes in lactate dehydrogenase (LDH) activity in PMN culture media when compared to untreated PMN (P = 0.689). In basal conditions, PMN of COPD patients released significantly more MMP-9 compared with PMN of healthy controls (P = 0.016). However, concentration ratio of MMP-9 released from PMN exposed to 4% CSE or 0% CSE of each participant was significantly higher for healthy subjects than for COPD patients (P = 0.025).
Conclusion: Cigarette smoke induces activation of PMN in healthy controls. However, chronically activated PMN in COPD patients could not be further stimulated by in vitro exposure to CSE. Constantly raised amount of MMP-9 released into the tissues may be involved in the degradation of extracellular matrix in the lungs as seen in COPD patients.

Relevance
Cigarette smoke induces the activation of polymorphonuclear leukocytes. This can have a negative impact on the occurrence of chronic obstructive pulmonary disease, and it is necessary to act preventively to reduce smoking. Physical activity can contribute to a reduced need to smoke and prevent oxidative and other pathophysiological mechanisms which contribute to the development of chronic lung disease