ABSTRACT
BACKGROUND AND OBJECTIVES: Mucin hypersecretion is one of the main symptoms of inflammatory diseases in the respiratory tract. The authors previously reported that pleiotypic pro-inflammatory cytokine, interleukin (IL)-1beta, plays significant roles in the respiratory tract inflammation by inducing mucins (MUC2, MUC5AC, MUC8). However, the molecular mechanism for mucin hypersecretion in the respiratory tract is still unclear. MATERIALS AND METHOD: 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 2-dimensional polyacrylamide gel electrophoresis (2-D PAGE) proteomics and cDNA microarray analysis (8.6 K). RESULTS: In the 2-D PAGE, 8 differentially expressed proteins and 14 post-translational modification proteins were identified 6 and 24 hrs after the IL-1beta treatment. Microarray analysis identified a total of 413 genes (6.6%) in the 6-hour treatment group and 115 genes (2.0%) in the 24-hour treatment group that were regulated after the IL-1beta treatment. The differentially expressed genes that were regulated by the IL-1beta treatment were mostly found in the metabolic pathway rather than in the regulatory pathway. A comparison of the proteomic and microarray data showed that there was a large discrepancy between the protein expression and the gene expression levels. Among the genes encoding the proteins secreted in the airway, MUC5B was down-regulated but sialomucin CD 164, lysozyme, and the secretory leukocyte protease inhibitor (SLPI) were up-regulated. CONCLUSION: These results clearly show that the transcript levels have little value in predicting the extent of protein expression. Genomics and proteomics have different evaluation fields. Therefore, they may not provide all the information on the gene and protein profiles.