RESEARCH Open Access Oxidative stress induced Interleukin-32 mRNA expression in human bronchial epithelial cells

Background: Chronic obstructive pulmonary disease (COPD) is characterized by airflow obstruction and persistent inflammation in the airways and lung parenchyma. Oxidative stress contributes to the pathogenesis of COPD. Interleukin (IL)-32 expression has been reported to increase in the lung tissue of patients with COPD. Here, we show that IFNg upregulated IL-32 expression and that oxidative stress augmented IFNg-induced-IL-32 expression in airway epithelial cells. We further investigated transcriptional regulation responsible for IFNg induced IL-32 expression in human airway epithelial cells. Methods: Human bronchial epithelial (HBE) cells were stimulated with H2O2 and IFNg, and IL-32 expression was evaluated. The cell viability was confirmed by MTT assay. The intracellular signaling pathways regulating IL-32 expression were investigated by examining the regulatory effects of MAPK inhibitors and JAK inhibitor after treatment with H2O2 and IFNg, and by using a ChIP assay to identify transcription factors (i.e. c-Jun, CREB) binding to the IL-32 promoter. Promoter activity assays were conducted after mutations were introduced into binding sites of c-Jun and CREB in the IL-32 promoter. IL-32 expression was also examined in HBE cells in which the expression of either c-Jun or CREB was knocked out by siRNA of indicated transcription factors. Results: There were no significant differences of cell viability among groups. After stimulation with H2O2 or IFN