Imperial College London
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ProfessorWendyBarclay

Faculty of Medicine, Department of Infectious Disease

Action Medical Research Chair Virology. Head of Department
 
 
 
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Contact

 

+44 (0)20 7594 5035w.barclay

 
 
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Location

 

416Medical SchoolSt Mary's Campus

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Summary

 

Publications

Citation

BibTex format

@article{Burnham:2022,
author = {Burnham, KL and Maher, AK and Jones, EM and Tan, MMH and Saputil, RC and Baillon, L and Selck, C and Giang, N and Arguello, R and Pillay, C and Thorley, E and Short, CE and Quinlan, R and Barclay, WS and Cooper, N and Taylor, GP and Davenport, EE and Dominguez-Villar, M},
journal = {Nature Communications},
pages = {1--17},
title = {Transcriptional reprogramming from innate immune functions to a pro-thrombotic signature by monocytes in COVID-19},
url = {https://www.nature.com/articles/s41467-022-35638-y},
volume = {13},
year = {2022}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - 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.
AU  - Burnham,KL
AU  - Maher,AK
AU  - Jones,EM
AU  - Tan,MMH
AU  - Saputil,RC
AU  - Baillon,L
AU  - Selck,C
AU  - Giang,N
AU  - Arguello,R
AU  - Pillay,C
AU  - Thorley,E
AU  - Short,CE
AU  - Quinlan,R
AU  - Barclay,WS
AU  - Cooper,N
AU  - Taylor,GP
AU  - Davenport,EE
AU  - Dominguez-Villar,M
EP  - 17
PY  - 2022///
SN  - 2041-1723
SP  - 1
TI  - Transcriptional reprogramming from innate immune functions to a pro-thrombotic signature by monocytes in COVID-19
T2  - Nature Communications
UR  - https://www.nature.com/articles/s41467-022-35638-y
UR  - http://hdl.handle.net/10044/1/101044
VL  - 13
ER  -
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