Previous studies have shown that tuberculosis (TB) is a risk factor for chronic airflow limitation. Chronic obstructive pulmonary disease (COPD) is recognized as the result of chronic inflammation, usually related to noxious particles. Post-TB airflow obstruction and tobacco-related COPD have the same functional pathway characterized by persistent airflow limitation. We sought to compare the profile of 29 cytokines in the sputum of subjects with post-TB airflow obstruction and those with COPD related to tobacco. The forced expiratory volume in the first second (FEV1) and forced expiratory volume/forced vital capacity (FEV/FVC) ratio were lower in the COPD patients with the history of smoking compared to the post-TB airflow obstruction subgroup. The stages of the disease were more advanced in COPD / tobacco patients. Among the cytokines, IL-1α, IL-1β, MIP-1β, sCD40L and VEGF levels were higher in COPD patients, compared to the controls with p values ​​of 0.003, 0.0001, 0.03, 0.0001 and 0.02 respectively. When the two COPD subgroups were compared, IL-1α, IL-6, TNF-α and IL-8 levels were higher in the COPD patients with the history of tobacco compared to the COPD patients with the history of TB with p-values ​​of 0.031, 0.05, 0.021 and 0.016, respectively. COPD related to tobacco is more severe than post-TB airflow obstruction. The pathogenesis of post-TB airflow obstruction appears to involve the cytokines IL-1RA, IL-1α, IL-1β, IL-17, GRO and sCD40L, while COPD related to tobacco involves more cytokines.

中文翻译：

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结核病后气流阻塞受试者和烟草相关慢性阻塞性肺病受试者痰液中的细胞因子谱

先前的研究表明，结核病（TB）是慢性气流受限的危险因素。慢性阻塞性肺病 (COPD) 被认为是慢性炎症的结果，通常与有毒颗粒有关。结核病后气流阻塞和烟草相关的慢性阻塞性肺病具有相同的功能途径，其特征是持续气流受限。我们试图比较结核病后气流阻塞受试者和烟草相关慢性阻塞性肺病受试者痰液中 29 种细胞因子的分布。与结核病后气流阻塞亚组相比，有吸烟史的COPD患者第一秒用力呼气量（FEV1）和用力呼气量/用力肺活量（FEV/FVC）比值较低。慢性阻塞性肺病/烟草患者的疾病阶段更为晚期。在细胞因子中，与对照组相比，COPD患者的IL-1α、IL-1β、MIP-1β、sCD40L和VEGF水平较高，p值分别为0.003、0.0001、0.03、0.0001和0.02。比较两个 COPD 亚组时，有烟草史的 COPD 患者的 IL-1α、IL-6、TNF-α 和 IL-8 水平高于有结核病史的 COPD 患者（p 值）​分别为 0.031、0.05、0.021 和 0.016。与烟草相关的慢性阻塞性肺病比结核病后气流阻塞更严重。结核病后气流阻塞的发病机制似乎涉及细胞因子IL-1RA、IL-1α、IL-1β、IL-17、GRO和sCD40L，而与烟草相关的COPD涉及更多细胞因子。