Abstract
Background Recent studies suggest that leptin is involved in Th2 response in allergic rhinitis (AR). However, the effect of leptin on type II innate lymphoid cells (ILC2s) in AR is not well characterized. Methods Twenty-six AR patients and 20 healthy controls were enrolled. Serum leptin levels were measured, and their correlation with ILC2 and type II cytokines were analyzed using enzyme-linked immunosorbent assay (ELISA) and flow cytometry. ILC2 differentiation and cytokine production stimulated by human recombinant leptin were analyzed by real-time polymerase chain reaction (PCR) and ELISA. AR mouse models were also established to verify the effect of leptin on ILC2 cell regulation. Results Our results showed that elevated serum leptin in AR patients was correlated with the percentage of ILC2 and the expression of type II cytokines. The recombinant leptin enhanced the expression of ILC2 cell transcription factors and type II cytokine through the PI3K/AKT pathway. The AR mice treated with leptin showed as stronger ILC2 inflammation and symptoms compared with control mice. Conclusions Our data provide evidence that upregulation of leptin promotes ILC2 responses in AR and this process was achieved through the PI3K/AKT pathway.
Highlights
Recent studies suggest that leptin is involved in Th2 response in allergic rhinitis (AR)
The serum levels of leptin in the AR group were significantly higher compared with control (9:8 ± 2:3 ng/mL vs.3:6 ± 1:5 ng/mL, P < 0:05)
The frequency of ILC2, IL-4+ ILC2, IL-5+ ILC2, and IL-13+ ILC2 was significantly elevated in AR patients compared with controls (Figures 1 and 2)
Summary
Recent studies suggest that leptin is involved in Th2 response in allergic rhinitis (AR). The effect of leptin on type II innate lymphoid cells (ILC2s) in AR is not well characterized. Serum leptin levels were measured, and their correlation with ILC2 and type II cytokines were analyzed using enzymelinked immunosorbent assay (ELISA) and flow cytometry. Our results showed that elevated serum leptin in AR patients was correlated with the percentage of ILC2 and the expression of type II cytokines. The recombinant leptin enhanced the expression of ILC2 cell transcription factors and type II cytokine through the PI3K/AKT pathway. Our data provide evidence that upregulation of leptin promotes ILC2 responses in AR and this process was achieved through the PI3K/AKT pathway. Previous studies have shown that the serum levels of leptin in patients with AR are significantly higher and positively correlated with the severity of clinical symptoms [8, 9]. The combination of leptin and its receptor activates JAK2-STAT3, MAPK, and PI3K-AKT pathways [10, 11]
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