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Locally organised and activated Fth1hi neutrophils aggravate inflammation of acute lung injury in an IL-10-dependent manner

Author

Listed:
  • Kun Wang

    (Tongji University School of Medicine)

  • Muyun Wang

    (Tongji University School of Medicine)

  • Ximing Liao

    (Tongji University School of Medicine)

  • Shaoyong Gao

    (Tongji University School of Medicine)

  • Jing Hua

    (Tongji University School of Medicine)

  • Xiaodong Wu

    (Tongji University School of Medicine)

  • Qian Guo

    (Tongji University School of Medicine)

  • Wujian Xu

    (Tongji University School of Medicine)

  • Jiaxing Sun

    (Tongji University School of Medicine)

  • Yanan He

    (Tongji University School of Medicine)

  • Qiang Li

    (Tongji University School of Medicine)

  • Wei Gao

    (Tongji University School of Medicine)

Abstract

Acute respiratory distress syndrome (ARDS) is a common respiratory critical syndrome with no effective therapeutic intervention. Neutrophils function in the overwhelming inflammatory process of acute lung injury (ALI) caused by ARDS; however, the phenotypic heterogeneity of pulmonary neutrophils in ALI/ARDS remains largely unknown. Here, using single-cell RNA sequencing, we identify two transcriptionally and functionally heterogeneous neutrophil populations (Fth1hi Neu and Prok2hi Neu) with distinct locations in LPS-induced ALI mouse lungs. Exposure to LPS promotes the Fth1hi Neu subtype, with more inflammatory factors, stronger antioxidant, and decreased apoptosis under the regulation of interleukin-10. Furthermore, prolonged retention of Fth1hi Neu within lung tissue aggravates inflammatory injury throughout the development of ALI/ARDS. Notably, ARDS patients have high ratios of Fth1 to Prok2 expression in pulmonary neutrophils, suggesting that the Fth1hi Neu population may promote the pathological development and provide a marker of poor outcome.

Suggested Citation

  • Kun Wang & Muyun Wang & Ximing Liao & Shaoyong Gao & Jing Hua & Xiaodong Wu & Qian Guo & Wujian Xu & Jiaxing Sun & Yanan He & Qiang Li & Wei Gao, 2022. "Locally organised and activated Fth1hi neutrophils aggravate inflammation of acute lung injury in an IL-10-dependent manner," Nature Communications, Nature, vol. 13(1), pages 1-19, December.
    • Handle: RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-35492-y
    DOI: 10.1038/s41467-022-35492-y
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    References listed on IDEAS

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    1. Dachuan Zhang & Grace Chen & Deepa Manwani & Arthur Mortha & Chunliang Xu & Jeremiah J. Faith & Robert D. Burk & Yuya Kunisaki & Jung-Eun Jang & Christoph Scheiermann & Miriam Merad & Paul S. Frenette, 2015. "Neutrophil ageing is regulated by the microbiome," Nature, Nature, vol. 525(7570), pages 528-532, September.
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    Cited by:

    1. Huirui Wang & Xiaona You & Jingcheng Wang & Xinyi Chen & Yinghui Gao & Mengmeng Wang & Wenru Zhang & Jiaozhen Zhang & Yang Yu & Bo Han & Mei Qi & Xiaohui Liu & Hongxiang Lou & Ting Dong, 2024. "MFSD7C protects hemolysis-induced lung impairments by inhibiting ferroptosis," Nature Communications, Nature, vol. 15(1), pages 1-17, December.
    2. Jiaoling Chen & Yaxing Bai & Ke Xue & Zhiguo Li & Zhenlai Zhu & Qingyang Li & Chen Yu & Bing Li & Shengxian Shen & Pei Qiao & Caixia Li & Yixin Luo & Hongjiang Qiao & Erle Dang & Wen Yin & Johann E. G, 2023. "CREB1-driven CXCR4hi neutrophils promote skin inflammation in mouse models and human patients," Nature Communications, Nature, vol. 14(1), pages 1-21, December.

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