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Activation of Complement Components on Circulating Blood Monocytes From COVID-19 Patients

  1. Author:
    Lage, Silvia Lucena
    Rocco, Joseph M
    Laidlaw, Elizabeth
    Rupert,Adam
    Galindo, Frances
    Kellogg,Anela
    Kumar, Princy
    Poon, Rita
    Wortmann, Glenn W
    Lisco, Andrea
    Manion, Maura
    Sereti, Irini

  2. Author Address

    HIV Pathogenesis Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States., AIDS Monitoring Laboratory, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research, Inc., Frederick, MD, United States., Clinical Monitoring Research Program Directorate, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research, Inc., Frederick, MD, United States., Division of Infectious Diseases and Tropical Medicine, Georgetown University Medical Center, Washington, DC, United States., Division of Hospital Medicine at MedStar Georgetown University Hospital, Washington, DC, United States., Section of Infectious Diseases, MedStar Washington Hospital Center, Washington, DC, United States.,
    1. Year: 2022
    2. Date: Feb 17
    3. Epub Date: 2022 02 17
  2. Journal: Frontiers in Immunology
    1. 13
    2. Pages: 815833
  4. Type of Article: Article
  5. Article Number: 815833
  1. Abstract:

    The coronavirus disease-2019 (COVID-19) caused by the SARS-CoV-2 virus may vary from asymptomatic to severe infection with multi-organ failure and death. Increased levels of circulating complement biomarkers have been implicated in COVID-19-related hyperinflammation and coagulopathy. We characterized systemic complement activation at a cellular level in 49-patients with COVID-19. We found increases of the classical complement sentinel C1q and the downstream C3 component on circulating blood monocytes from COVID-19 patients when compared to healthy controls (HCs). Interestingly, the cell surface-bound complement inhibitor CD55 was also upregulated in COVID-19 patient monocytes in comparison with HC cells. Monocyte membrane-bound C1q, C3 and CD55 levels were associated with plasma inflammatory markers such as CRP and serum amyloid A during acute infection. Membrane-bounds C1q and C3 remained elevated even after a short recovery period. These results highlight systemic monocyte-associated complement activation over a broad range of COVID-19 disease severities, with a compensatory upregulation of CD55. Further evaluation of complement and its interaction with myeloid cells at the membrane level could improve understanding of its role in COVID-19 pathogenesis. Copyright © 2022 Lage, Rocco, Laidlaw, Rupert, Galindo, Kellogg, Kumar, Poon, Wortmann, Lisco, Manion and Sereti.

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External Sources

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  2. DOI: 10.3389/fimmu.2022.815833
  3. PMID: 35250994
  4. PMCID: PMC8892247

Library Notes

  1. Fiscal Year: FY2021-2022
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