Piezo1-Induced Nasal Epithelial Barrier Dysfunction in Allergic Rhinitis

This study aimed to investigate the role of Piezo1 in nasal epithelial barrier dysfunction in allergic rhinitis (AR) using both in vitro and in vivo experimental methods. A total of 79 human nasal mucosal samples were collected, including 43 from AR patients and 36 from healthy controls. Additionally, 12 BALB/c mice were used for the in vivo experiments. Human nasal epithelial cells (HNEpCs) were employed for the in vitro studies. In the in vivo study, mice were sensitized with ovalbumin (OVA) to induce AR. In the in vitro experiments, Piezo1 expression in HNEpCs was silenced using shRNA, followed by stimulation with IL-13. The expression of Piezo1, ERK1/2, and tight junctions (TJs) components (including ZO-1, Occludin, and Claudin-1) was assessed using quantitative RT-PCR, immunofluorescence, and Western blotting. Statistical analyses included paired Student's t-test and one-way ANOVA. Piezo1 expression was significantly elevated in both AR patients and OVA-induced AR mice, while TJs components were significantly reduced (p < 0.05). Knockdown of Piezo1 in HNEpCs restored the levels of TJs and improved barrier integrity. A negative correlation between Piezo1 and ERK1/2 expression was observed. Piezo1 plays a crucial role in nasal epithelial barrier dysfunction in AR by modulating TJs and the ERK1/2 pathway. These findings suggest that Piezo1 may serve as a potential therapeutic target for AR.