Liu Zhizhen, Chen Siyang, Xu Yongjian, Liu Xiansheng, Xiong Pian, Fu Yu
Department of Respiratory Medicine, Yiwu Fuyuan Hospital.
Department of Cardiothoracic Surgery, The Fourth Affiliated Hospital, Zhejiang University School of Medicine, Yiwu.
Medicine (Baltimore). 2020 Feb;99(7):e19118. doi: 10.1097/MD.0000000000019118.
Cigarette smoking is considered the main risk factor for chronic obstructive pulmonary disease (COPD), although the mechanism remains unknown. surfactant protein A (SP-A) is thought to protect the lung from smoking-induced damage, but related studies performed in China are scarce. The aim of the study is to assess alterations of SP-A expression and distribution in lung samples from Chinese smokers with or without COPD.This cross-sectional study assessed 45 men in Wuhan Tongji Hospital after lobectomy for lung cancer in June 2010 to September 2010. Peripheral lung specimens were collected from control nonsmokers without airflow obstruction (nonsmoking group, n = 15), smokers without airflow obstruction (smoking group, n = 15), and patients with COPD (COPD group, n = 15). SP-A expression levels in lung tissue samples and its distribution in lung cells, type II pneumocytes (PNII), and alveolar macrophages (MACR) were determined by immunoblotting and immunohistochemistry.SP-A levels were significantly decreased in the COPD group (1.00 ± 0.25) compared with the smoking (2.31 ± 0.64) and nonsmoking (8.03 ± 2.80) groups; the smoking group also showed significantly reduced levels compared with the nonsmoking group (P < .05). PNII expressing SP-A were less abundant in the COPD group (39.3% ± 7.1%) compared with the smoking group (76.2% ± 29.8%), whereas SP-A MACR were more abundant (92.4% ± 7.1% vs 68.5% ± 20.2%) (all P < .05). Among the 30 smokers, forced expiratory volume in one second (% predicted) was positively correlated with SP-A levels (r = 0.739) and the rate of SP-A+ PNII (r = 0.811), and negatively correlated with the rate of SP-A+ MACR (r = -0.758) (all P < .05).Changes in SP-A expression and distribution in lung tissues may be involved in COPD pathogenesis in smokers.
吸烟被认为是慢性阻塞性肺疾病（COPD）的主要危险因素，但其机制尚不清楚。表面活性蛋白A（SP-A）被认为可保护肺部免受吸烟引起的损伤，但在中国进行的相关研究较少。本研究旨在评估有或无COPD的中国吸烟者肺组织样本中SP-A表达和分布的变化。这项横断面研究评估了2010年6月至2010年9月在武汉同济医院接受肺癌肺叶切除术后的45名男性。从无气流阻塞的对照非吸烟者（非吸烟组，n = 15）、无气流阻塞的吸烟者（吸烟组，n = 15）和COPD患者（COPD组，n = 15）中采集外周肺标本。通过免疫印迹和免疫组织化学测定肺组织样本中SP-A的表达水平及其在肺细胞、II型肺泡上皮细胞（PNII）和肺泡巨噬细胞（MACR）中的分布。与吸烟组（2.31±0.64）和非吸烟组（8.03±2.80）相比，COPD组的SP-A水平显著降低（1.00±0.25）；与非吸烟组相比，吸烟组的水平也显著降低（P <.05）。与吸烟组（76.2%±29.8%）相比，COPD组中表达SP-A的PNII较少（39.3%±7.1%），而表达SP-A的MACR较多（92.4%±7.1%对68.5%±20.2%）（所有P <.05）。在30名吸烟者中，一秒用力呼气量（%预测值）与SP-A水平（r = 0.739）和SP-A+PNII的比例（r = 0.811）呈正相关，与SP-A+MACR的比例呈负相关（r = -0.758）（所有P <.05）。肺组织中SP-A表达和分布的变化可能参与了吸烟者COPD的发病机制。
