Serapinas Danielius, Narbekovas Andrius, Juskevicius Jonas, Sakalauskas Raimundas
Department of Pulmonology and Immunology, Medical Academy, Lithuanian University of Health Sciences, Kaunas, Lithuania.
Multidiscip Respir Med. 2011 Aug 31;6(4):214-9. doi: 10.1186/2049-6958-6-4-214.
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.
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 concentrations.
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).
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.
吸烟是慢性阻塞性肺疾病（COPD）发生的主要危险因素，COPD最近被定义为一种全身性肺部炎症性疾病。然而，吸烟本身对COPD患者全身炎症的影响尚未完全明确。我们研究的目的是调查炎症标志物与吸烟状况之间的关联。
我们比较了202名现吸烟者、61名既往吸烟者和57名从不吸烟者，他们均为COPD患者。评估内容包括病史、肺功能测定、α-1抗胰蛋白酶（AAT）基因分型、血清AAT、C反应蛋白（CRP）、肿瘤坏死因子（TNF）-α以及可溶性肿瘤坏死因子受体（sTNFR）-1和sTNFR-2浓度。
吸烟者（1.75±0.51 g/L和14.4[9.5 - 20.5]mg/L）和既往吸烟者（1.69±0.43 g/L和12.3[8.7 - 16.3]mg/L）的AAT和CRP浓度高于从不吸烟者（1.49±0.38 g/L和5.1[2.5 - 8.7]mg/L；p<0.05）。吸烟者的sTNFR-1水平高于既往吸烟者或从不吸烟者（241.2 pg/mL[145.3 - 349.4] vs. 213.7 pg/mL[147.1 - 280.3]和205.2 pg/mL[125 - 275]；p<0.05）。
我们的数据证实，吸烟与COPD患者体内AAT、CRP和sTNFR-1水平升高有关，这些全身性炎症标志物即使在戒烟后仍保持活跃。
