Leptin Promoted IL-17 Production from ILC2s in Allergic Rhinitis

Background. Interleukin-17 plays important roles in allergic diseases. Several studies proved that leptin promoted Th17 immune responses by inducing RORγt transcription. ILC2 is an important member of the early stage of immune response. Therefore, we aimed to explore the effect of leptin on the IL-1...

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Main Authors: Yanhui Wen, Qingxiang Zeng, Xi Luo, Renqiang Ma, Yiquan Tang, Wenlong Liu
Format: Article
Language:English
Published: Wiley 2020-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2020/9248479
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author Yanhui Wen
Qingxiang Zeng
Xi Luo
Renqiang Ma
Yiquan Tang
Wenlong Liu
author_facet Yanhui Wen
Qingxiang Zeng
Xi Luo
Renqiang Ma
Yiquan Tang
Wenlong Liu
author_sort Yanhui Wen
collection DOAJ
description Background. Interleukin-17 plays important roles in allergic diseases. Several studies proved that leptin promoted Th17 immune responses by inducing RORγt transcription. ILC2 is an important member of the early stage of immune response. Therefore, we aimed to explore the effect of leptin on the IL-17 production by ILC2 in AR in this study. Methods. Fifteen AR patients and fifteen healthy controls were enrolled. Serum leptin levels were measured, and their correlation with the frequency of IL-17+ ILC2 cells was analyzed using enzyme-linked immunosorbent assay (ELISA) and flow cytometry. ILC2 was stimulated by leptin, and the expression of IL-17, IL-5, and IL-13 was detected by ELISA. The correlated pathways were confirmed by real-time PCR. Results. We found that serum leptin and the frequency of IL-17-producing ILC2s in AR were significantly higher compared with those in controls. After being incubated with leptin, the frequency of IL-17+ ILC2 cells and IL-17 production from ILC2 was upregulated compared with that in controls. We also found that leptin induced RORγt and Ahr expression by ILC2. Moreover, leptin-induced IL-17-producing ILC2 concomitantly expressed IL-5 and IL-13. Conclusions. Our data provide preliminary evidence that leptin-induced IL-17 production from ILC2 cells is dependent on RORγt and Ahr expression and the blockade of leptin may be a promising target for the treatment of AR.
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spelling doaj-art-f5ef96f11c124314be60ebd2063bf2962025-02-03T05:57:19ZengWileyMediators of Inflammation0962-93511466-18612020-01-01202010.1155/2020/92484799248479Leptin Promoted IL-17 Production from ILC2s in Allergic RhinitisYanhui Wen0Qingxiang Zeng1Xi Luo2Renqiang Ma3Yiquan Tang4Wenlong Liu5Department of Otolaryngology, Dongguan Songshan Lake Center Hospital, Dongguan, 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 Otorhinolaryngology, Otorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen 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. Interleukin-17 plays important roles in allergic diseases. Several studies proved that leptin promoted Th17 immune responses by inducing RORγt transcription. ILC2 is an important member of the early stage of immune response. Therefore, we aimed to explore the effect of leptin on the IL-17 production by ILC2 in AR in this study. Methods. Fifteen AR patients and fifteen healthy controls were enrolled. Serum leptin levels were measured, and their correlation with the frequency of IL-17+ ILC2 cells was analyzed using enzyme-linked immunosorbent assay (ELISA) and flow cytometry. ILC2 was stimulated by leptin, and the expression of IL-17, IL-5, and IL-13 was detected by ELISA. The correlated pathways were confirmed by real-time PCR. Results. We found that serum leptin and the frequency of IL-17-producing ILC2s in AR were significantly higher compared with those in controls. After being incubated with leptin, the frequency of IL-17+ ILC2 cells and IL-17 production from ILC2 was upregulated compared with that in controls. We also found that leptin induced RORγt and Ahr expression by ILC2. Moreover, leptin-induced IL-17-producing ILC2 concomitantly expressed IL-5 and IL-13. Conclusions. Our data provide preliminary evidence that leptin-induced IL-17 production from ILC2 cells is dependent on RORγt and Ahr expression and the blockade of leptin may be a promising target for the treatment of AR.http://dx.doi.org/10.1155/2020/9248479
spellingShingle Yanhui Wen
Qingxiang Zeng
Xi Luo
Renqiang Ma
Yiquan Tang
Wenlong Liu
Leptin Promoted IL-17 Production from ILC2s in Allergic Rhinitis
Mediators of Inflammation
title Leptin Promoted IL-17 Production from ILC2s in Allergic Rhinitis
title_full Leptin Promoted IL-17 Production from ILC2s in Allergic Rhinitis
title_fullStr Leptin Promoted IL-17 Production from ILC2s in Allergic Rhinitis
title_full_unstemmed Leptin Promoted IL-17 Production from ILC2s in Allergic Rhinitis
title_short Leptin Promoted IL-17 Production from ILC2s in Allergic Rhinitis
title_sort leptin promoted il 17 production from ilc2s in allergic rhinitis
url http://dx.doi.org/10.1155/2020/9248479
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AT qingxiangzeng leptinpromotedil17productionfromilc2sinallergicrhinitis
AT xiluo leptinpromotedil17productionfromilc2sinallergicrhinitis
AT renqiangma leptinpromotedil17productionfromilc2sinallergicrhinitis
AT yiquantang leptinpromotedil17productionfromilc2sinallergicrhinitis
AT wenlongliu leptinpromotedil17productionfromilc2sinallergicrhinitis