목적: Eosinophilic chronic rhinosinusitis with nasal polyps (eCRSwNP) is characterized by persistent sinus inflammation and severe eosinophil infiltration. While the relationship between eosinophil infiltration and nasal poly formation has been extensively studied, the specific mechanisms underlying eosinophil infiltration into the nasal epithelium remain unclear. In a preliminary study, we identified an upregulation of cadherin 26(CDH26) – one of the epithelial adhesion molecules - in eCRSwNP patients through analysis of published single-cell RNA sequencing data. Therefore, we aimed to investigate the potential role and mechanism of CDH26 in the transepithelial migration of eosinophil into the nasal mucosa of eCRSwNP patients. 방법:Immunohistochemistry(IHC) was performed on tissues from eCRSwNP patient, non-eCRSwNP patient, CRSsNP patients, and healthy control to assess CDH26 expression. The expression of CDH26 in human nasal epithelial cells (HNECs) and air-liquid interface(ALI) cultures in response to inflammatory cytokines was analyzed using real-time polymerase chain reaction(RT-PCR), Western-blotting, and IHC. Dupilumab, an interleukin 4 (IL-4) receptor inhibitor, was applied to HNEC monolayer cultures to investigate the signaling pathway. ITGA4 expression on EoL-1, an eosinophil cell line, was evaluated via flow cytometry, and the interaction between recombinant CDH26 protein and EoL-1 cells was assessed using a cell adhesion assay. 결과:IHC confirmed that CDH26 expression was elevated exclusively in eCRSwNP patient. CDH26 expression in HNECs was significantly upregulated following treatment with IL-4 and IL-13, as demonstrated by RT-PCR and IHC. This upregulation was reversed in a dose-dependent manner with Dupilumab treatment. Flow cytometry revealed ITGA4 expression on EoL-1 cells, and the cell adhesion assay demonstrated the attachment of EoL-1 cells to recombinant CDH26. 결론:Our findings suggest that upregulation of CDH26 on Th2 cytokine- activated epithelial cells facilitates the transepithelial migration of eosinophils through ITGA4. This mechanism provides a new perspective on potential therapeutic targets for patients with eCRSwNP.