목적: CRSwNP which were belongs to a Th2 type inflammatory disorders were known to be a refractory clinical disease. HIFs which have basic helix-loop-helix structures has an important roles orchestrating cellular responses like energy switch, cell movement, angiogenesis. Most of all, HIFs could be a main players in nasal polypogenesis via Epithelial to Mesenchymal Transition. Recently, class III NAD+ dependent histone deacetylase(SIRT1) has been known to suppresses HIF-1. Thus we hypothesized that Sirt1 could possibly attenuates nasal polypogensis by inhibiting HIF-1 mediated EMT. 방법:Immnublotting was utilized to evaluate the EMT, HIF1A in hNEC(human nasal epithelial cell) and RPMI2650 cell lines, respectively. Reporter assays were used to assess the HIF1a transcription activities. Tissue extract were prepared from nasal tissues of UP, CRSsNP, CRSwNP(eosinophilic) and CRSwNP(Non-eosinophilic) each. The total protein concentrations in each of the extracts were measured using Bradford assay. 결과:CRSwNP(non-eosinophilic) extract shows much lower level of SIRT1 rather than those from CRSwNP(eosinophilic). Under hypoxic incubation conditions, CRS mucosal extract treatment enhanced the SIRT1 level, which suppressed the expression of HIF-1α and PDK1 also. In connection with this fact, IFN-gamma and TNF-alpha which were both epithelial derived non-eosinophilic cytokines induce EMT significantly in nasal epithelial cells than IL-17A and IL-5 which were eosinophilic cytokines. 결론: Loss of SIRT1 in CRS patients likely to contribute to the formation of the nasal polypogenesis and could possibly thought to be a new therapeutic target for nasal polyp. Especially, asian polyp(non-eosinophilic) cytokines which were known to different types of cytokines comparison with those of western polyp(eosinophilic) shows more powerful EMT effect in nasal epithelial cells. It suggested that different kinds of approach method were needed to treat nasal polyp.