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Updated: Aug 11, 2026

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
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The microglial NLRP3 inflammasome is involved in human SARS-CoV-2 cerebral pathogenicity: A report of three

Viviana Falcón Cama1, Javier Marín-Prida2, Nelson Acosta-Rivero3

  • 1Center for Genetic Engineering and Biotechnology (CIGB), Ave. 31 e/158 y 190, Cubanacán, Playa, PO Box 6162, Havana, Cuba; Latin American School of Medicine, Carretera Panamericana Km 3 1/2, Playa, Havana, 11600, Cuba..

Journal of Neuroimmunology
|October 7, 2021
PubMed

Insights

SARS-CoV-2 nucleocapsid and its entry receptor ACE2 were found in brain cells of deceased COVID-19 patients. The NLRP3 inflammasome, implicated in SARS-CoV-2 lesions, suggests a potential therapeutic target.

Area of Science:

  • Neurology
  • Immunology
  • Virology

Background:

  • COVID-19, caused by SARS-CoV-2, can affect the central nervous system.
  • Understanding the neuropathological mechanisms of SARS-CoV-2 is crucial for patient outcomes.

Observation:

  • Confocal immunofluorescence detected SARS-CoV-2 nucleocapsid in neurons, astrocytes, oligodendrocytes, and microglia in post-mortem brain tissue.
  • The viral nucleocapsid colocalized with the ACE2 receptor, the primary entry point for SARS-CoV-2.
  • NLRP3 inflammasome activation was observed in cerebral cortical tissues and colocalized with CD68+ macrophages in the brain and lung.

Findings:

  • SARS-CoV-2 infects multiple brain cell types, including neurons and glial cells.
  • The presence of ACE2 indicates the mechanism of viral entry into these cells.
  • NLRP3 inflammasome activation is a key feature in SARS-CoV-2-affected brain and lung tissues.

Implications:

  • These findings highlight the direct impact of SARS-CoV-2 on the nervous system.
  • NLRP3 inflammasome activation presents a potential therapeutic target for mitigating SARS-CoV-2-induced neuropathology and lung injury.
Keywords:
COVID-19Human brainMacrophagesNLRP3 inflammasomeSARS-CoV-2

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