Solar ultraviolet B radiation promotes α-MSH secretion to attenuate the function of ILC2s via the pituitary–lung axis

Abstract The immunomodulatory effects of ultraviolet B (UVB) radiation in human diseases have been described. Whether type 2 lung inflammation is directly affected by solar ultraviolet (UV) radiation is not fully understood. Here, we show a possible negative correlation between solar UVB radiation a...

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出版年:Nature Communications
主要な著者: Yuying Huang, Lin Zhu, Shipeng Cheng, Ranran Dai, Chunrong Huang, Yanyan Song, Bo Peng, Xuezhen Li, Jing Wen, Yi Gong, Yunqian Hu, Ling Qian, Linyun Zhu, Fengying Zhang, Li Yu, Chunyan Yi, Wangpeng Gu, Zhiyang Ling, Liyan Ma, Wei Tang, Li Peng, Guochao Shi, Yaguang Zhang, Bing Sun
フォーマット: 論文
言語:英語
出版事項: Nature Portfolio 2023-09-01
オンライン・アクセス:https://doi.org/10.1038/s41467-023-41319-1
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author Yuying Huang
Lin Zhu
Shipeng Cheng
Ranran Dai
Chunrong Huang
Yanyan Song
Bo Peng
Xuezhen Li
Jing Wen
Yi Gong
Yunqian Hu
Ling Qian
Linyun Zhu
Fengying Zhang
Li Yu
Chunyan Yi
Wangpeng Gu
Zhiyang Ling
Liyan Ma
Wei Tang
Li Peng
Guochao Shi
Yaguang Zhang
Bing Sun
author_facet Yuying Huang
Lin Zhu
Shipeng Cheng
Ranran Dai
Chunrong Huang
Yanyan Song
Bo Peng
Xuezhen Li
Jing Wen
Yi Gong
Yunqian Hu
Ling Qian
Linyun Zhu
Fengying Zhang
Li Yu
Chunyan Yi
Wangpeng Gu
Zhiyang Ling
Liyan Ma
Wei Tang
Li Peng
Guochao Shi
Yaguang Zhang
Bing Sun
author_sort Yuying Huang
collection DOAJ
container_title Nature Communications
description Abstract The immunomodulatory effects of ultraviolet B (UVB) radiation in human diseases have been described. Whether type 2 lung inflammation is directly affected by solar ultraviolet (UV) radiation is not fully understood. Here, we show a possible negative correlation between solar UVB radiation and asthmatic inflammation in humans and mice. UVB exposure to the eyes induces hypothalamus-pituitary activation and α-melanocyte-stimulating hormone (α-MSH) accumulation in the serum to suppress allergic airway inflammation by targeting group 2 innate lymphoid cells (ILC2) through the MC5R receptor in mice. The α-MSH/MC5R interaction limits ILC2 function through attenuation of JAK/STAT and NF-κB signaling. Consistently, we observe that the plasma α-MSH concentration is negatively correlated with the number and function of ILC2s in the peripheral blood mononuclear cells (PBMC) of patients with asthma. We provide insights into how solar UVB radiation-driven neuroendocrine α-MSH restricts ILC2-mediated lung inflammation and offer a possible strategy for controlling allergic diseases.
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spelling doaj-art-80db1dee153a4e9c8ed1d1f9f7bed0be2025-08-19T22:15:46ZengNature PortfolioNature Communications2041-17232023-09-0114111610.1038/s41467-023-41319-1Solar ultraviolet B radiation promotes α-MSH secretion to attenuate the function of ILC2s via the pituitary–lung axisYuying Huang0Lin Zhu1Shipeng Cheng2Ranran Dai3Chunrong Huang4Yanyan Song5Bo Peng6Xuezhen Li7Jing Wen8Yi Gong9Yunqian Hu10Ling Qian11Linyun Zhu12Fengying Zhang13Li Yu14Chunyan Yi15Wangpeng Gu16Zhiyang Ling17Liyan Ma18Wei Tang19Li Peng20Guochao Shi21Yaguang Zhang22Bing Sun23State Key Laboratory of Cell Biology, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of SciencesState Key Laboratory of Cell Biology, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of SciencesState Key Laboratory of Cell Biology, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of SciencesDepartment of Pulmonary and Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of MedicineDepartment of Pulmonary and Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of MedicineDepartment of Biostatistics, Clinical Research Institute, Shanghai Jiao Tong University School of MedicineDepartment of Pulmonary and Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of MedicineState Key Laboratory of Cell Biology, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of SciencesState Key Laboratory of Cell Biology, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of SciencesHuashan Hospital Affiliated to Fudan UniversityDepartment of Pulmonary and Critical Care Medicine, Shanghai East Hospital, School of Medicine, Tongji UniversityDepartment of Pulmonary and Critical Care Medicine, Shanghai Fifth People’s Hospital, Fudan UniversityShanghai Putuo District Central HospitalShanghai Putuo District People’s HospitalDepartment of Pulmonary and Critical Care Medicine, Tongji Hospital, School of Medicine, Tongji UniversityState Key Laboratory of Cell Biology, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of SciencesState Key Laboratory of Cell Biology, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of SciencesState Key Laboratory of Cell Biology, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of SciencesState Key Laboratory of Cell Biology, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of SciencesDepartment of Pulmonary and Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of MedicineShanghai Key Laboratory of Meteorology and Health, Shanghai Meteorological ServiceDepartment of Pulmonary and Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of MedicineState Key Laboratory of Cell Biology, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of SciencesState Key Laboratory of Cell Biology, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of SciencesAbstract The immunomodulatory effects of ultraviolet B (UVB) radiation in human diseases have been described. Whether type 2 lung inflammation is directly affected by solar ultraviolet (UV) radiation is not fully understood. Here, we show a possible negative correlation between solar UVB radiation and asthmatic inflammation in humans and mice. UVB exposure to the eyes induces hypothalamus-pituitary activation and α-melanocyte-stimulating hormone (α-MSH) accumulation in the serum to suppress allergic airway inflammation by targeting group 2 innate lymphoid cells (ILC2) through the MC5R receptor in mice. The α-MSH/MC5R interaction limits ILC2 function through attenuation of JAK/STAT and NF-κB signaling. Consistently, we observe that the plasma α-MSH concentration is negatively correlated with the number and function of ILC2s in the peripheral blood mononuclear cells (PBMC) of patients with asthma. We provide insights into how solar UVB radiation-driven neuroendocrine α-MSH restricts ILC2-mediated lung inflammation and offer a possible strategy for controlling allergic diseases.https://doi.org/10.1038/s41467-023-41319-1
spellingShingle Yuying Huang
Lin Zhu
Shipeng Cheng
Ranran Dai
Chunrong Huang
Yanyan Song
Bo Peng
Xuezhen Li
Jing Wen
Yi Gong
Yunqian Hu
Ling Qian
Linyun Zhu
Fengying Zhang
Li Yu
Chunyan Yi
Wangpeng Gu
Zhiyang Ling
Liyan Ma
Wei Tang
Li Peng
Guochao Shi
Yaguang Zhang
Bing Sun
Solar ultraviolet B radiation promotes α-MSH secretion to attenuate the function of ILC2s via the pituitary–lung axis
title Solar ultraviolet B radiation promotes α-MSH secretion to attenuate the function of ILC2s via the pituitary–lung axis
title_full Solar ultraviolet B radiation promotes α-MSH secretion to attenuate the function of ILC2s via the pituitary–lung axis
title_fullStr Solar ultraviolet B radiation promotes α-MSH secretion to attenuate the function of ILC2s via the pituitary–lung axis
title_full_unstemmed Solar ultraviolet B radiation promotes α-MSH secretion to attenuate the function of ILC2s via the pituitary–lung axis
title_short Solar ultraviolet B radiation promotes α-MSH secretion to attenuate the function of ILC2s via the pituitary–lung axis
title_sort solar ultraviolet b radiation promotes α msh secretion to attenuate the function of ilc2s via the pituitary lung axis
url https://doi.org/10.1038/s41467-023-41319-1
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