Systemic inflammation in COPD in relation to smoking status

Background and aims: Smoking is the main risk factor for the development of chronic obstructive pulmonary disease (COPD) that has been recently defined as a systemic pulmonary inflammatory disease. However, the impact of smoking itself on systemic inflammation in COPD patients has not yet been well established. The aim of our study was to investigate the association between inflammatory markers and smoking status. Material and methods: We compared 202 current smokers, 61 ex-smokers and 57 never-smokers, all COPD patients. Assessments included medical history, spirometry, alpha-1 antitrypsin (AAT) genotyping, serum AAT, C-reactive protein (CRP), tumor necrosis factor (TNF)-alpha, and soluble tumor necrosis factor receptor (5TNFR)-1 and sTNFR-2 concentrations. Results: AAT and CRP concentrations in smokers (1.75 +/- 0.51 g/L and 14.4 [9.5-20.5] mg/L) and ex-smokers (1.69 +/- 0.43 g/L and 12.3 [8.7-16.3] mg/L) were higher than in never-smokers (1.49 +/- 0.38 g/L and 5.1 [2.5-8.7] mg/L; p < 0.05). sTNFR-1 level was higher in smokers than ex-smokers or never-smokers (241.2 pg/mL [145.3-349.4] vs. 213.7 pg/mL [147.1-280.3] and 205.2 pg/mL [125-275]; p < 0.05). Conclusions: Our data confirm that smoking is associated with increased levels of AAT, CRP, and sTNFR-1 in COPD patients, an array of systemic inflammation markers that continue to be active even after smoking cessation.