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

Silvia Lucena Lage1, Joseph M Rocco1, Elizabeth Laidlaw1

  • 1HIV Pathogenesis Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States.

Frontiers in Immunology
|March 7, 2022
PubMed

Insights

Complement activation on monocytes is increased in COVID-19 patients, with higher levels of C1q and C3. This monocyte-associated complement activation and CD55 upregulation persist post-infection, suggesting a role in COVID-19 pathogenesis.

Area of Science:

  • Immunology
  • Infectious Diseases
  • Cell Biology

Background:

  • Coronavirus disease-2019 (COVID-19) can lead to severe outcomes including multi-organ failure.
  • Elevated complement biomarkers are linked to COVID-19 hyperinflammation and coagulopathy.

Purpose of the Study:

  • To characterize systemic complement activation at the cellular level in COVID-19 patients.
  • To investigate the expression of complement components and inhibitors on monocytes during COVID-19.

Main Methods:

  • Flow cytometry was used to analyze complement components (C1q, C3) and inhibitors (CD55) on circulating monocytes.
  • Comparison was made between 49 COVID-19 patients and healthy controls (HCs).
  • Association with inflammatory markers (CRP, serum amyloid A) was assessed.

Main Results:

  • COVID-19 patients showed increased C1q and C3 on monocytes compared to HCs.
  • Monocytes from COVID-19 patients also exhibited upregulated cell surface-bound CD55.
  • Elevated membrane-bound C1q, C3, and CD55 correlated with inflammatory markers during acute infection.
  • C1q and C3 remained elevated on monocytes after a recovery period.

Conclusions:

  • Systemic complement activation involving monocytes occurs broadly across COVID-19 severity.
  • A compensatory upregulation of CD55 on monocytes is observed in COVID-19.
  • Further research into complement-myeloid cell interactions is crucial for understanding COVID-19 pathogenesis.

Keywords:
COVID-19complementinflammationmonocytessurface expression

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