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Mechanics-activated fibroblasts promote pulmonary group 2 innate lymphoid cell plasticity propelling silicosis progression

Author

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  • Yangyang He

    (Key Laboratory of Environmental Stress and Chronic Disease Control & Prevention (China Medical University), Ministry of Education
    China Medical University
    University of Texas Health Science Center San Antonio)

  • Fan Yang

    (Key Laboratory of Environmental Stress and Chronic Disease Control & Prevention (China Medical University), Ministry of Education
    China Medical University)

  • Lin Yang

    (Key Laboratory of Environmental Stress and Chronic Disease Control & Prevention (China Medical University), Ministry of Education
    China Medical University)

  • Haoyang Yuan

    (Key Laboratory of Environmental Stress and Chronic Disease Control & Prevention (China Medical University), Ministry of Education
    China Medical University)

  • Yichuan You

    (Key Laboratory of Environmental Stress and Chronic Disease Control & Prevention (China Medical University), Ministry of Education
    China Medical University)

  • Yinghui Chen

    (Key Laboratory of Environmental Stress and Chronic Disease Control & Prevention (China Medical University), Ministry of Education
    China Medical University)

  • Xiulin Wu

    (Key Laboratory of Environmental Stress and Chronic Disease Control & Prevention (China Medical University), Ministry of Education
    China Medical University)

  • Hui Min

    (China Medical University)

  • Jie Chen

    (Key Laboratory of Environmental Stress and Chronic Disease Control & Prevention (China Medical University), Ministry of Education
    China Medical University)

  • Chao Li

    (Key Laboratory of Environmental Stress and Chronic Disease Control & Prevention (China Medical University), Ministry of Education
    China Medical University)

Abstract

Crystalline silica (CS) particle exposure leads to silicosis which is characterized as progressive fibrosis. Fibroblasts are vital effector cells in fibrogenesis. Emerging studies have identified immune sentinel roles for fibroblasts in chronic disease, while their immune-modulatory roles in silicosis remain unclear. Herein, we show that group 2 innate lymphoid cell (ILC2) conversion to ILC1s is closely involved in silicosis progression, which is mediated by activated fibroblasts via interleukin (IL)−18. Mechanistically, Notch3 signaling in mechanics-activated fibroblasts modulates IL-18 production via caspase 1 activity. The mouse-specific Notch3 knockout in fibroblasts retards pulmonary fibrosis progression that is linked to attenuated ILC conversion. Our results indicate that activated fibroblasts in silicotic lungs are regulators of ILC2–ILC1 conversion, associated with silicosis progression via the Notch3–IL-18 signaling axis. This finding broadens our understanding of immune-modulatory mechanisms in silicosis, and indicates potential therapeutic targets for lung fibrotic diseases.

Suggested Citation

  • Yangyang He & Fan Yang & Lin Yang & Haoyang Yuan & Yichuan You & Yinghui Chen & Xiulin Wu & Hui Min & Jie Chen & Chao Li, 2024. "Mechanics-activated fibroblasts promote pulmonary group 2 innate lymphoid cell plasticity propelling silicosis progression," Nature Communications, Nature, vol. 15(1), pages 1-18, December.
    • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-54174-5
    DOI: 10.1038/s41467-024-54174-5
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    References listed on IDEAS

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    1. Hongdong Wang & Lei Shen & Xitai Sun & Fangcen Liu & Wenhuan Feng & Chunping Jiang & Xuehui Chu & Xiao Ye & Can Jiang & Yan Wang & Pengzi Zhang & Mengwei Zang & Dalong Zhu & Yan Bi, 2019. "Adipose group 1 innate lymphoid cells promote adipose tissue fibrosis and diabetes in obesity," Nature Communications, Nature, vol. 10(1), pages 1-14, December.
    2. Kevin Wei & Ilya Korsunsky & Jennifer L. Marshall & Anqi Gao & Gerald F. M. Watts & Triin Major & Adam P. Croft & Jordan Watts & Philip E. Blazar & Jeffrey K. Lange & Thomas S. Thornhill & Andrew File, 2020. "Notch signalling drives synovial fibroblast identity and arthritis pathology," Nature, Nature, vol. 582(7811), pages 259-264, June.
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