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

The clinical respiratory journal

PubMedID: 24761997

Rong Y, Xiang XD, Li YM, Peng ZY, Li JX. IL-32 was involved in cigarette smoke induced pulmonary inflammation in COPD. Clin Respir J. 2014;.
PURPOSE
Previous study has proved the over-expression of interleukin 32 (IL-32) in COPD lungs. 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 which 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 between 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 FEV1/FVC 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 TNF-a). 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.