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

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-Eve Short, Rachael Quinlan, Wendy S. Barclay, Nichola Cooper, Graham P. Taylor, Emma E. Davenport and Margarita Dominguez-Villar ()
Additional contact information
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

Nature Communications, 2022, vol. 13, issue 1, 1-17

Abstract: 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.

Date: 2022
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DOI: 10.1038/s41467-022-35638-y

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