Mucin hypersecretion is one of the main symptoms of inflammatory disease in the respiratory tract. We previously reported that the pleiotypic pro-inflammatory cytokine, interleukin (IL)-1beta, plays a significant role in respiratory tract inflammation by inducing mucins. However, the molecular mechanism for mucin hypersecretion in the respiratory tract remains still unclear. In order to understand the mechanisms of mucin hypersecretion in the airway epithelium, the differentially expressed proteins and genes in the lung mucoepidermoid carcinoma cell line (NCI-H292 cells), which were treated for 6 and 24 hours with IL-1beta (10 ng/mL) were identified using two-dimensional polyacrylamide gel electrophoresis (2-D PAGE) proteomics and cDNA microarray analysis (8.6K). In the 2-D PAGE, eight differentially expressed proteins and 14 post-translational modification proteins were identified at 6 and 24 hours after the IL-1beta-treatment. Four hundred and thirteen genes (6.6%) and 115 genes (2.0%) were differentially expressed, respectively, at 6 and 24 hours after the IL-1beta-treatment by microarray analysis. The differentially expressed genes and proteins that were regulated by the IL-1beta-treatment were mostly in the metabolic pathway rather than in the regulatory pathway. These results clearly show that the transcript levels have little value in predicting the extent of protein expression.