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Transcriptional reprogramming from innate immune functions to a pro-thrombotic signature by monocytes in COVID-19

Author

Listed:
  • Allison K. Maher

    (Imperial College London)

  • Katie L. Burnham

    (Wellcome Genome Campus, Hinxton)

  • Emma M. Jones

    (Imperial College London)

  • Michelle M. H. Tan

    (Imperial College London)

  • Rocel C. Saputil

    (Imperial College London)

  • Laury Baillon

    (Imperial College London)

  • Claudia Selck

    (Imperial College London)

  • Nicolas Giang

    (Imperial College London)

  • Rafael Argüello

    (Centre d’Immunologie de Marseille-Luminy)

  • Clio Pillay

    (Imperial College London)

  • Emma Thorley

    (Imperial College London)

  • Charlotte-Eve Short

    (Imperial College London)

  • Rachael Quinlan

    (Imperial College London)

  • Wendy S. Barclay

    (Imperial College London)

  • Nichola Cooper

    (Imperial College London)

  • Graham P. Taylor

    (Imperial College London)

  • Emma E. Davenport

    (Wellcome Genome Campus, Hinxton)

  • Margarita Dominguez-Villar

    (Imperial College London)

Abstract

Although alterations in myeloid cells have been observed in COVID-19, the specific underlying mechanisms are not completely understood. Here, we examine the function of classical CD14+ monocytes in patients with mild and moderate COVID-19 during the acute phase of infection and in healthy individuals. Monocytes from COVID-19 patients display altered expression of cell surface receptors and a dysfunctional metabolic profile that distinguish them from healthy monocytes. Secondary pathogen sensing ex vivo leads to defects in pro-inflammatory cytokine and type-I IFN production in moderate COVID-19 cases, together with defects in glycolysis. COVID-19 monocytes switch their gene expression profile from canonical innate immune to pro-thrombotic signatures and are functionally pro-thrombotic, both at baseline and following ex vivo stimulation with SARS-CoV-2. Transcriptionally, COVID-19 monocytes are characterized by enrichment of pathways involved in hemostasis, immunothrombosis, platelet aggregation and other accessory pathways to platelet activation and clot formation. These results identify a potential mechanism by which monocyte dysfunction may contribute to COVID-19 pathology.

Suggested Citation

  • Allison K. Maher & Katie L. Burnham & Emma M. Jones & Michelle M. H. Tan & Rocel C. Saputil & Laury Baillon & Claudia Selck & Nicolas Giang & Rafael Argüello & Clio Pillay & Emma Thorley & Charlotte-E, 2022. "Transcriptional reprogramming from innate immune functions to a pro-thrombotic signature by monocytes in COVID-19," Nature Communications, Nature, vol. 13(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-35638-y
    DOI: 10.1038/s41467-022-35638-y
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    Cited by:

    1. Tristram A. J. Ryan & Alexander Hooftman & Aisling M. Rehill & Matt D. Johansen & Eóin C. O’ Brien & Juliana E. Toller-Kawahisa & Mieszko M. Wilk & Emily A. Day & Hauke J. Weiss & Pourya Sarvari & Emi, 2023. "Dimethyl fumarate and 4-octyl itaconate are anticoagulants that suppress Tissue Factor in macrophages via inhibition of Type I Interferon," Nature Communications, Nature, vol. 14(1), pages 1-15, December.

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