목적: IL-33 plays an important role in controlling immune responses in barrier tissues and is a potent mediator of diverse inflammatory disease such as asthma, rheumatoid diseases and chronic rhinosinusitis. The purposes of present study are to evaluate production of IL-33 by proinflammatory cytokine in nasal epithelial cells and A549 and to find which stimulation is important for the secretion of IL-33 in airway epithelium and investigated the underlying mechanism of action. 방법:Primary nasal epithelial cells (PNEC) from 5 normal patients were incubated. RT-PCR, ELISA and immunofluorescence staining was performed for IL-33 production to identify which proinflammatory cytokine stimulates production of IL-33. Three MAP kinases (p38, extracellular signal-regulated kinase [ERK], c-Jun N-terminal kinase [JNK]) and NF-κB were evaluated as downstream signaling molecules by RT-PCR, ELISA, western blot analysis and Luciferase reporter assay. 결과:The level of IL-33 mRNA and protein expression increased significantly by TNF-α but not by interferon-γ, IL-1β and transforming growth factor-β1 in PNEC and A549 cells. TNF-α stimulates the expression of IL-33 in dose and time-dependent in A549 cells. PNEC and A549 cells were treated with TNF-α with specific inhibitors of p38, ERK, JNK and NF-κB. In both cells, inhibitors of ERK, p38 and NF-κB reversed the increased expression of IL-33 by TNF-α. In luciferase reporter assay, activity of NF-κB was inhibited by not only NF-κB but also ERK and p38 inhibitor. 결론:The results of the present study showed that TNF-α stimulates IL- 33 expression through ERK, p38 and NFκB pathway in PNEC and A549.