Systemic inflammation in COPD in relation to smoking status

Abstract

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 pul- monary inflammatory disease. However, the impact of smok- ing itself on systemic inflammation in COPD patients has not yet been well established. The aim of our study was to inves- tigate 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)-α, and soluble tumor necrosis factor receptor (sTNFR)-1 and sTNFR-2 concentra- tions.

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-smok- ers (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.