2. Academic Validation
  3. Solar ultraviolet B radiation promotes α-MSH secretion to attenuate the function of ILC2s via the pituitary-lung axis

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

  • Nat Commun. 2023 Sep 12;14(1):5601. doi: 10.1038/s41467-023-41319-1.
Yuying Huang # 1,  Lin Zhu # 1,  Shipeng Cheng # 1,  Ranran Dai # 2,  Chunrong Huang # 2,  Yanyan Song 3,  Bo Peng 2,  Xuezhen Li 1,  Jing Wen 1,  Yi Gong 4,  Yunqian Hu 5,  Ling Qian 6,  Linyun Zhu 7,  Fengying Zhang 8,  Li Yu 9,  Chunyan Yi 1,  Wangpeng Gu 1,  Zhiyang Ling 1,  Liyan Ma 1,  Wei Tang 10,  Li Peng 11,  Guochao Shi 12,  Yaguang Zhang 13 14,  Bing Sun 15
Affiliations

Affiliations

  • 1 State 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 Sciences, Shanghai, China.
  • 2 Department of Pulmonary and Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  • 3 Department of Biostatistics, Clinical Research Institute, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  • 4 Huashan Hospital Affiliated to Fudan University, Shanghai, China.
  • 5 Department of Pulmonary and Critical Care Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.
  • 6 Department of Pulmonary and Critical Care Medicine, Shanghai Fifth People's Hospital, Fudan University, Shanghai, China.
  • 7 Shanghai Putuo District Central Hospital, Shanghai, China.
  • 8 Shanghai Putuo District People's Hospital, Shanghai, China.
  • 9 Department of Pulmonary and Critical Care Medicine, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
  • 10 Department of Pulmonary and Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. tina_tangwei@163.com.
  • 11 Shanghai Key Laboratory of Meteorology and Health, Shanghai Meteorological Service, Shanghai, China. phyllis_pl@163.com.
  • 12 Department of Pulmonary and Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. shiguochao@hotmail.com.
  • 13 State 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 Sciences, Shanghai, China. zhangyaguang@sibcb.ac.cn.
  • 14 Med-X Institute, Center for Immunological and Metabolic Diseases, The First Affiliated Hospital of Xi'an JiaoTong University, Xi'an JiaoTong University, Xi'an, Shaanxi, P. R. China. zhangyaguang@sibcb.ac.cn.
  • 15 State 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 Sciences, Shanghai, China. bsun@sibs.ac.cn.
  • # Contributed equally.
PMID: 37699899 DOI: 10.1038/s41467-023-41319-1
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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