Activation of Complement Components on Circulating Blood Monocytes From COVID-19 Patients.
Activation of Complement Components on Circulating Blood Monocytes From COVID-19 Patients.
- 2022
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.
English
1664-3224
10.3389/fimmu.2022.815833 [doi] PMC8892247 [pmc]
*Complement Activation/im [Immunology]
*Complement System Proteins/im [Immunology]
*COVID-19/im [Immunology]
*Monocytes/im [Immunology]
Adult
Adult
Biomarkers/bl [Blood]
Complement Inactivating Agents/im [Immunology]
COVID-19/bl [Blood]
COVID-19/vi [Virology]
Cytokines/im [Immunology]
Female
Humans
Immunologic Factors/im [Immunology]
Male
Middle Aged
Monocytes/vi [Virology]
SARS-CoV-2/im [Immunology]
MedStar Washington Hospital Center
Medicine/Infectious Diseases
Journal Article
Research Support, N.I.H., Intramural
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.
English
1664-3224
10.3389/fimmu.2022.815833 [doi] PMC8892247 [pmc]
*Complement Activation/im [Immunology]
*Complement System Proteins/im [Immunology]
*COVID-19/im [Immunology]
*Monocytes/im [Immunology]
Adult
Adult
Biomarkers/bl [Blood]
Complement Inactivating Agents/im [Immunology]
COVID-19/bl [Blood]
COVID-19/vi [Virology]
Cytokines/im [Immunology]
Female
Humans
Immunologic Factors/im [Immunology]
Male
Middle Aged
Monocytes/vi [Virology]
SARS-CoV-2/im [Immunology]
MedStar Washington Hospital Center
Medicine/Infectious Diseases
Journal Article
Research Support, N.I.H., Intramural