Budesonide inhibits interleukin-32 expression in a rat model of chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder of the lung, and is the fifth leading cause of morbidity worldwide. A novel proinflammatory factor, interleukine-32 (IL-32), is suggested as a risk factor of COPD. Budesonide is widely used for COPD treatment as anti-inflammatory drug. However, the inflammatory inhibition mechanism of budesonide is not fully understood. In this study, we used a rat model with COPD to investigate the effect of budesonide on IL-32 expression in lung tissue. We found that cigarette smoking (CS) strongly induced IL-32 expression in lung tissue, seriously weakened lung function, and damaged pulmonary tissue. Budesonide inhibited the expression of IL-32 in lung tissue. In budesonide-treated rats, we observed no repair of damaged lung tissue but the pulmonary function was partly recovered. To our knowledge, this is the first report that budesonide inhibits the expression of IL-32 in lung tissues, which is strongly induced by CS.