Leptin Regulated ILC2 Cell through the PI3K/AKT Pathway in Allergic Rhinitis

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 wer...

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Main Authors: Qingxiang Zeng, Xi Luo, Yiquan Tang, Wenlong Liu, Renzhong Luo
Format: Article
Language:English
Published: Wiley 2020-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2020/4176082
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author Qingxiang Zeng
Xi Luo
Yiquan Tang
Wenlong Liu
Renzhong Luo
author_facet Qingxiang Zeng
Xi Luo
Yiquan Tang
Wenlong Liu
Renzhong Luo
author_sort Qingxiang Zeng
collection DOAJ
description 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.
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series Mediators of Inflammation
spelling doaj-art-dd0a6cd5dfb24f148e1f8d2f4e2a336d2025-08-20T02:21:38ZengWileyMediators of Inflammation0962-93511466-18612020-01-01202010.1155/2020/41760824176082Leptin Regulated ILC2 Cell through the PI3K/AKT Pathway in Allergic RhinitisQingxiang Zeng0Xi Luo1Yiquan Tang2Wenlong Liu3Renzhong Luo4Department of Otolaryngology, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou, ChinaDepartment of Otolaryngology, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou, ChinaDepartment of Otolaryngology, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou, ChinaDepartment of Otolaryngology, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou, ChinaDepartment of Otolaryngology, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou, ChinaBackground. 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.http://dx.doi.org/10.1155/2020/4176082
spellingShingle Qingxiang Zeng
Xi Luo
Yiquan Tang
Wenlong Liu
Renzhong Luo
Leptin Regulated ILC2 Cell through the PI3K/AKT Pathway in Allergic Rhinitis
Mediators of Inflammation
title Leptin Regulated ILC2 Cell through the PI3K/AKT Pathway in Allergic Rhinitis
title_full Leptin Regulated ILC2 Cell through the PI3K/AKT Pathway in Allergic Rhinitis
title_fullStr Leptin Regulated ILC2 Cell through the PI3K/AKT Pathway in Allergic Rhinitis
title_full_unstemmed Leptin Regulated ILC2 Cell through the PI3K/AKT Pathway in Allergic Rhinitis
title_short Leptin Regulated ILC2 Cell through the PI3K/AKT Pathway in Allergic Rhinitis
title_sort leptin regulated ilc2 cell through the pi3k akt pathway in allergic rhinitis
url http://dx.doi.org/10.1155/2020/4176082
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AT yiquantang leptinregulatedilc2cellthroughthepi3kaktpathwayinallergicrhinitis
AT wenlongliu leptinregulatedilc2cellthroughthepi3kaktpathwayinallergicrhinitis
AT renzhongluo leptinregulatedilc2cellthroughthepi3kaktpathwayinallergicrhinitis