INTRODUCTION: Chronic obstructive pulmonary disease (COPD) is a worldwide burden 
and a major cause of death. The disease is accompanied by chronic inflammation 
and increased cellular turnover that is partly due to an overwhelming induction 
of apoptosis. In this study, we hypothesized that systemic markers of apoptosis 
are altered in patients with mild-to-severe COPD.
MATERIALS AND METHODS: A total number of 64 patients and controls were enrolled 
in the study. Lung function parameters of all groups (nonsmoker, healthy smoker, 
COPD GOLD I&II, COPD GOLD III&IV) were evaluated at the time of inclusion. 
Enzyme-linked immunosorbent assays were used to quantify protein levels in serum 
samples.
RESULTS: Serum contents of apoptotic end-products caspase-cleaved cytokeratin-18 
and histone-associated-DNA-fragments were increased in patients with COPD, 
whereas anti-inflammatory soluble ST2 showed a peak in patients with COPD I&II 
(P=0.031) compared to healthy smokers. Levels of pro-inflammatory caspase-1/ ICE 
correlated significantly with the number of pack years (R=0.337; P=0.007).
DISCUSSION: Our results indicate a systemic release of apoptosis-specific 
proteins as markers for increased cellular turnover accompanied by progression 
of COPD. Furthermore, soluble ST2 seems to have a critical role in the 
anti-inflammatory regulatory mechanism at early stages of the disease.