IL-32 was involved in cigarette smoke-induced pulmonary inflammation in COPD

• Published in: The clinical respiratory journal 2015-10, Vol.9 (4), p.430-435
• Main Authors: Rong, Yao, Xiang, Xu-dong, Li, Ya-min, Peng, Zhen-yu, Li, Jin-xiu
• Format: Article
• Language: English
• Subjects: Aged; Case-Control Studies; Cells, Cultured; Chronic obstructive pulmonary disease; COPD; Emphysema; Female; Humans; inflammation; interleukin 32; Interleukins - biosynthesis; Interleukins - blood; Macrophages - drug effects; Macrophages - pathology; Male; Middle Aged; Pneumonia - blood; Pneumonia - etiology; Pneumonia - pathology; Pulmonary Disease, Chronic Obstructive - blood; Pulmonary Disease, Chronic Obstructive - etiology; Pulmonary Disease, Chronic Obstructive - pathology; smoke; Smoking - adverse effects; Smoking - blood; Sputum - metabolism; Up-Regulation
• ISSN: 1752-6981; 1752-699X
• DOI: 10.1111/crj.12157

Purpose Previous study has proven the overexpression of interleukin 32 (IL‐32) in lungs with chronic obstructive pulmonary disease (COPD). But the soluble IL‐32 levels and the role of IL‐32 in smokers and COPD are still unclear. Methods In this study, we enrolled 133 subjects who were divided into three groups: nonsmokers, control smokers and smokers with COPD. We detected the IL‐32 levels in serum and induced sputum of all subjects. The pulmonary function, PaO2 and smoking exposure index were also collected. Moreover, macrophages were isolated and stimulated by cigarette smoke extraction (CSE). A special siRNA was used to suppress the IL‐32 expression. Results There was no significant difference in IL‐32 serum levels among the three groups. The IL‐32 levels of induced sputum in COPD patients were markedly higher than control smokers and nonsmokers. The IL‐32 levels in induced sputum of COPD patients were negatively correlated with forced expiratory volume (FEV1)/forced vital capacity and FEV1%. Moreover, a low concentration CSE could stimulate IL‐32 expression and promote the release of several inflammatory factors (such as IL‐6 and tumor necrosis factor‐α). A special siRNA could significantly suppress the release of these inflammatory factors. Conclusions This study revealed the critical role of IL‐32 in pulmonary inflammation of COPD and smoker‐associated diseases.