[High mobility group box1 contributes to hypoxia-induced barrier dysfunction of nasal epithelial cells].

: Objective:To investigated the promotion of high mobility group box1 (HMGB1) under hypoxia, and determined the regulatory role of HMGB1 on the barrier function of nasal epithelial cells.Method:Primary nasal epithelial cells (NECs) collected from patients with septal deviation were cultured at air-liquid interface. The release of HMGB1 under hypoxia was detected by ELISA. The effect of HMGB1 on fluorescein isothiocyanatedextran 4 kDa (FD4) permeability of NECs was measured. Western blot analysis was utilized to examine the level of major junction proteins, namely E-cadherin, ZO-1, Occludin and Claudin-1.Result:The release of HMGB1 was significantly upregulated in NECs under hypoxia. Recombinant human HMGB1 increased FD4 permeability in a dose and time-dependent manner, indicating the impaired epithelial barrier function. HMGB1-mediated barrier hyperpermeability was accompanied by the selective downregulation of ZO-1, occludin and Claudin-1, but not E-cadherin.Conclusion:HMGB1 mediates hypoxia-induce barrier dysfunction of nasal epithelium, which may be a potential target for the treatment of chronic rhinosinusitis.