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Real-time Live-cell Flow Cytometry to Investigate Calcium Influx, Pore Formation, and Phagocytosis by P2X7 Receptors in Adult Neural Progenitor Cells
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The potential involvement of P2X7 receptor in COVID-19 pathogenesis: A new therapeutic target?

Paulo A F Pacheco1, Robson X Faria1

  • 1Laboratório de Toxoplasmose e outras Protozooses, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz, Rio de Janeiro, Brazil.

Scandinavian Journal of Immunology
|August 16, 2020
PubMed

Insights

The P2X7 receptor/NLRP3 inflammasome axis may drive immune dysregulation in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, contributing to COVID-19 pathogenesis through sustained cytokine production.

Area of Science:

  • Immunology
  • Pathogenesis
  • Molecular Biology

Background:

  • Coronavirus disease 2019 (COVID-19) pathogenesis involves immune system dysregulation.
  • Hyperinflammation, marked by sustained cytokine production like IL-1β, is a key feature.
  • Cytokine release and maturation depend on inflammasome activation, particularly NLRP3.

Purpose of the Study:

  • To explore the potential role of the P2X7 receptor/NLRP3 inflammasome axis in SARS-CoV-2 infection.
  • To investigate the link between P2X7R/NLRP3 activation and COVID-19 immune dysregulation.

Main Methods:

  • Literature review and evidence synthesis.
  • Analysis of molecular mechanisms underlying inflammasome activation.
  • Correlation of P2X7R/NLRP3 pathway with SARS-CoV-2 infection characteristics.

Main Results:

  • The P2X7 receptor (P2X7R) can be activated by extracellular ATP.
  • NLRP3 inflammasome activation, triggered by P2X7R, leads to IL-1β maturation and release.
  • Evidence suggests this axis contributes to the hyperinflammatory response observed in SARS-CoV-2 infections.

Conclusions:

  • The P2X7R/NLRP3 inflammasome pathway is a potential driver of immune dysregulation in COVID-19.
  • Targeting this axis could offer therapeutic strategies for managing SARS-CoV-2-induced hyperinflammation.
Keywords:
COVID-19NLRP3 inflammasomeP2X7 receptorSARS-CoV-2immunopathogenesis

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