IL-17A disrupts the nasal mucosal epithelial barrier in patients with chronic rhinosinusitis by activating the ERK/STAT3 pathway

The mucosal epithelial barrier, the first line of immune defense, is vulnerable to allergens, pathogens, and inflammatory cytokines, contributing to CRS development. Our previous studies found high interleukin-17A(IL-17A) expression correlated with CRS severity and low glucocorticoid efficacy. The role of IL-17A in disrupting the nasal mucosal epithelial barrier leading to CRS remains unclear. We aimed to investigate how IL-17A promoting epithelial barrier damage and identify new treatment targets for CRS.