tetano
Editor, Senior Moderator
Front Immunol
. 2022 Feb 17;13:815833.
doi: 10.3389/fimmu.2022.815833. eCollection 2022.
Activation of Complement Components on Circulating Blood Monocytes From COVID-19 Patients
Silvia Lucena Lage[SUP] 1 [/SUP], Joseph M Rocco[SUP] 1 [/SUP], Elizabeth Laidlaw[SUP] 1 [/SUP], Adam Rupert[SUP] 2 [/SUP], Frances Galindo[SUP] 1 [/SUP], Anela Kellogg[SUP] 3 [/SUP], Princy Kumar[SUP] 4 [/SUP], Rita Poon[SUP] 5 [/SUP], Glenn W Wortmann[SUP] 6 [/SUP], Andrea Lisco[SUP] 1 [/SUP], Maura Manion[SUP] 1 [/SUP], Irini Sereti[SUP] 1 [/SUP]
Affiliations
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.
Keywords: COVID-19; complement; inflammation; monocytes; surface expression.
. 2022 Feb 17;13:815833.
doi: 10.3389/fimmu.2022.815833. eCollection 2022.
Activation of Complement Components on Circulating Blood Monocytes From COVID-19 Patients
Silvia Lucena Lage[SUP] 1 [/SUP], Joseph M Rocco[SUP] 1 [/SUP], Elizabeth Laidlaw[SUP] 1 [/SUP], Adam Rupert[SUP] 2 [/SUP], Frances Galindo[SUP] 1 [/SUP], Anela Kellogg[SUP] 3 [/SUP], Princy Kumar[SUP] 4 [/SUP], Rita Poon[SUP] 5 [/SUP], Glenn W Wortmann[SUP] 6 [/SUP], Andrea Lisco[SUP] 1 [/SUP], Maura Manion[SUP] 1 [/SUP], Irini Sereti[SUP] 1 [/SUP]
Affiliations
- PMID: 35250994
- PMCID: PMC8892247
- DOI: 10.3389/fimmu.2022.815833
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.
Keywords: COVID-19; complement; inflammation; monocytes; surface expression.