A decreased expression of leptin receptor may contribute to the pathogenesis of the allergic rhinitis

Body: Background: Allergic rhinitis (AR) is characterized by an inflammation induced by the allergen exposure, with consequential structural abnormalities in the nasal epithelium. Thymic stromal lymphopoietin (TSLP) is an IL-7-like cytokine that plays a key role in the development of AR, as it was detected in the nasal epithelium of patients with allergic rhinitis but not in that of controls. On the other hand, leptin/leptin receptor pathway has been shown to be involved in the epithelial homeostasis. The specific role of the leptin/leptin receptor pathway in the homeostasis of nasal tissue is unknown. Aim: To determine whether a nasal epithelial dysfunction of leptin/leptin receptor pathway contributes to AR pathogenesis. Methods: The human nasal epithelial cell line RPMI 2650 was examined for the expression of leptin and leptin receptor by immunocytochemistry. Also the RPMI 2650 were cultured in the presence or absence of the major allergen of the Parietaria judaica pollen (rPar j 1) and of the fibrogenic cytokine TGF- 1 and were analyzed for leptin receptor and for TSLP expression by flow cytometry and by immunocytochemistry, respectively. Results: The human nasal epithelial cell line RPMI 2650 expresses leptin and leptin receptor. rPar j 1 and TGF- 1 significantly decreases the leptin receptor expression (p=0.001 and p=0.04 respectively). TSLP expression is induced in the RPMI 2650 cultured with rPar j 1 and with TGF- 1 in comparison to RPMI 2650 cultured in medium. Conclusions: Allergen exposure and fibrogenic cytokine TGF- 1 alter the homeostasis of nasal epithelium down-regulating leptin/leptin receptor pathway. Funded by Glaxo-SmithKline