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Integrated cytokine and metabolite analysis reveals immunometabolic reprogramming in COVID-19 patients with therapeutic implications

Author

Listed:
  • Nan Xiao

    (Tsinghua University)

  • Meng Nie

    (Tsinghua University
    Tsinghua University)

  • Huanhuan Pang

    (Tsinghua University
    Tsinghua University)

  • Bohong Wang

    (Tsinghua University
    Tsinghua University)

  • Jieli Hu

    (Chongqing Medical University)

  • Xiangjun Meng

    (Tsinghua University)

  • Ke Li

    (NHC Key Laboratory of Biotechnology of Antibiotics, Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences & Peking Union Medical College)

  • Xiaorong Ran

    (Agilent Technologies (China), Chaoyang District)

  • Quanxin Long

    (Chongqing Medical University)

  • Haijun Deng

    (Chongqing Medical University)

  • Na Chen

    (Tsinghua University)

  • Shao Li

    (Tsinghua University)

  • Ni Tang

    (Chongqing Medical University)

  • Ailong Huang

    (Chongqing Medical University)

  • Zeping Hu

    (Tsinghua University
    Tsinghua University
    Tsinghua University)

Abstract

Cytokine release syndrome (CRS) is a major cause of the multi-organ injury and fatal outcome induced by SARS-CoV-2 infection in severe COVID-19 patients. Metabolism can modulate the immune responses against infectious diseases, yet our understanding remains limited on how host metabolism correlates with inflammatory responses and affects cytokine release in COVID-19 patients. Here we perform both metabolomics and cytokine/chemokine profiling on serum samples from healthy controls, mild and severe COVID-19 patients, and delineate their global metabolic and immune response landscape. Correlation analyses show tight associations between metabolites and proinflammatory cytokines/chemokines, such as IL-6, M-CSF, IL-1α, IL-1β, and imply a potential regulatory crosstalk between arginine, tryptophan, purine metabolism and hyperinflammation. Importantly, we also demonstrate that targeting metabolism markedly modulates the proinflammatory cytokines release by peripheral blood mononuclear cells isolated from SARS-CoV-2-infected rhesus macaques ex vivo, hinting that exploiting metabolic alterations may be a potential strategy for treating fatal CRS in COVID-19.

Suggested Citation

  • Nan Xiao & Meng Nie & Huanhuan Pang & Bohong Wang & Jieli Hu & Xiangjun Meng & Ke Li & Xiaorong Ran & Quanxin Long & Haijun Deng & Na Chen & Shao Li & Ni Tang & Ailong Huang & Zeping Hu, 2021. "Integrated cytokine and metabolite analysis reveals immunometabolic reprogramming in COVID-19 patients with therapeutic implications," Nature Communications, Nature, vol. 12(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-21907-9
    DOI: 10.1038/s41467-021-21907-9
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    Cited by:

    1. Yongxian Hu & Jingjing Li & Fang Ni & Zhongli Yang & Xiaohua Gui & Zhiwei Bao & Houli Zhao & Guoqing Wei & Yiyun Wang & Mingming Zhang & Ruimin Hong & Linqin Wang & Wenjun Wu & Mohamad Mohty & Arnon N, 2022. "CAR-T cell therapy-related cytokine release syndrome and therapeutic response is modulated by the gut microbiome in hematologic malignancies," Nature Communications, Nature, vol. 13(1), pages 1-14, December.
    2. Yafeng Li & Jessica S. Hook & Qing Ding & Xue Xiao & Stephen S. Chung & Marcel Mettlen & Lin Xu & Jessica G. Moreland & Michalis Agathocleous, 2023. "Neutrophil metabolomics in severe COVID-19 reveal GAPDH as a suppressor of neutrophil extracellular trap formation," Nature Communications, Nature, vol. 14(1), pages 1-16, December.

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