Department of Internal Medicine, Pulmonology Division, Botucatu Medical School. UNESP (Paulista State University). Distrito de Rubião Júnior, s/n. Botucatu, 18618-000, SP, Brazil.
Department of Internal Medicine, Botucatu Medical School. UNESP (Paulista State University). Distrito de Rubião Júnior, s/n. Botucatu, 18618-000, SP, Brazil.
J Inflamm (Lond). 2010 Jun 9;7:29. doi: 10.1186/1476-9255-7-29.
Smoking cause airway and systemic inflammation and COPD patients present low grade inflammation in peripheral blood. However, data on the influence of smoking itself on systemic inflammation in COPD patients are scarce. This study investigated the association between inflammation, smoking status, and disease.
A cross-sectional analysis comparing 53 COPD ex-smokers, 24 COPD current smokers, 24 current smoker controls and 34 never-smoker controls was performed. Assessments included medical history, body composition, spirometry, and plasma concentration of tumor necrosis factor-alpha (TNF-alpha), interleukins (IL)-6, IL-8, and C-reactive protein (CRP).
Our exploratory analysis showed that serum TNF-alpha was higher in COPD current smokers [4.8(4.2-5.8)pg/mL] and in current smoker controls [4.8 (4.2-6.1) pg/mL] when compared to COPD ex-smokers [4.3 (3.9-4.9)pg/mL; p = 0.02] and to never-smoker controls [3.7 (3.4-4.0)pg/mL; p < 0.001]. Multiple regression results with and without adjustment for covariates were consistent with the hypothesis that TNF-alpha levels were associated with smoking status in both models (p < 0.001 and p < 0.001). IL-6 and CRP were significantly higher in COPD patients when compared to smoker and never-smoker controls and the multiple regression analysis confirmed the association of these mediators with disease, but not with smoking status (p < 0.001 and p < 0.001). IL-8 had only a borderline association with disease in both models (p = 0.069 and p = 0.053). No influence of disease severity, inhaled corticosteroid, fat-free mass (FFM) depletion and long term oxygen therapy (LTOT) use on systemic inflammation was found.
Smoking may influence TNF-alpha mediated systemic inflammation, which, in turn, may account for some of the benefits observed in patients with COPD who stop smoking.
吸烟可导致气道和全身炎症，COPD 患者外周血存在低度炎症。然而，关于吸烟本身对 COPD 患者全身炎症影响的数据却很少。本研究旨在探讨炎症、吸烟状态与疾病之间的关系。
进行了一项横断面分析，比较了 53 名 COPD 戒烟者、24 名 COPD 吸烟者、24 名现吸烟者对照组和 34 名从不吸烟者对照组。评估包括病史、人体成分、肺量测定和肿瘤坏死因子-α（TNF-α）、白细胞介素（IL）-6、IL-8 和 C 反应蛋白（CRP）的血浆浓度。
我们的探索性分析显示，与 COPD 戒烟者[4.3（3.9-4.9）pg/mL]相比，COPD 吸烟者[4.8（4.2-5.8）pg/mL]和现吸烟者对照组[4.8（4.2-6.1）pg/mL]的血清 TNF-α水平更高（p=0.02），与从不吸烟者对照组[3.7（3.4-4.0）pg/mL]相比更高（p<0.001）。有和没有调整协变量的多元回归结果均与 TNF-α水平与吸烟状态相关的假设一致，在两个模型中均具有统计学意义（p<0.001 和 p<0.001）。与吸烟者和从不吸烟者对照组相比，COPD 患者的 IL-6 和 CRP 显著升高，多元回归分析证实这些介质与疾病相关，而与吸烟状态无关（p<0.001 和 p<0.001）。IL-8 在两个模型中与疾病仅呈边缘相关（p=0.069 和 p=0.053）。未发现疾病严重程度、吸入性皮质类固醇、去脂体重（FFM）消耗和长期氧疗（LTOT）的使用对全身炎症有影响。
吸烟可能会影响 TNF-α介导的全身炎症，而这种炎症反过来可能是 COPD 患者戒烟后观察到一些益处的原因之一。
