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

MedStar author(s):

1664-3224

Name of journal: Frontiers in immunologyAbstract: 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.All authors: Galindo F, Kellogg A, Kumar P, Lage SL, Laidlaw E, Lisco A, Manion M, Poon R, Rocco JM, Rupert A, Sereti I, Wortmann GWOriginally published: Frontiers in Immunology. 13:815833, 2022.Fiscal year: FY2022Digital Object Identifier:

https://dx.doi.org/10.3389/fimmu.2022.815833

Date added to catalog: 2022-05-11

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Title notes ( 2 )

Holdings
Item type	Current library	Collection	Call number	Status	Date due	Barcode
Journal Article	MedStar Authors Catalog	Article	35250994	Available		35250994

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