Fluticasone furoate restores leptin/leptin receptor pathway in nasal epithelial cells

Leptin/leptin receptor pathway has been shown to be involved in the epithelial homeostasis and in tissue repair. Allergic rhinitis (AR) is characterized by a IgE-mediated inflammation induced by the allergen exposure, leading to a chronic inflammation with consequential structural abnormalities in the nasal epithelium. Topical corticosteroids are recommended as first-line therapy in AR. The role of the leptin/leptin receptor pathway and the specific effect of fluticasone furoate (FF), a new topical corticosteroid, in the homeostasis of nasal epithelial cells are largely unknown. We aimed to determine whether a nasal epithelial dysfunction of leptin/leptin receptor pathway contributes to AR pathogenesis and to investigate the effect of FF on this pathway. The human nasal epithelial cell line RPMI 2650 was first examined for leptin/leptin receptor expression by immunocytochemistry and by flow-cytometry. Then, the RPMI 2650 cells were cultured in the presence or absence of the allergen extract parietaria judaica (PARJ1), of the fibrogenic cytokine TGF-β1 and of FF and analyzed for leptin receptor by flow-citometry and for cell proliferation by clonogenic assay. The RPMI 2650 cells express leptin and leptin receptor. PARJ1 and TGF-β1 significantly decreases the leptin receptor expression and cell proliferation and FF completely abolishes and reverts the effects of both PARJ1 and TGF-β1. In conclusion, allergen exposure and TGF-β1 alter the homeostasis of nasal epithelium by down-regulating leptin/leptin receptor pathway whereas FF is able to restore both this pathway and nasal epithelial homeostasis.