Related Experiment Video

Updated: Aug 26, 2025

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
09:04

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells

Published on: May 22, 2014

21.0K

Interleukin-1 and the NLRP3 inflammasome in COVID-19: Pathogenetic and therapeutic implications

Nicola Potere1, Marco Giuseppe Del Buono2, Roberto Caricchio3

  • 1Department of Medicine and Ageing Sciences and Department of Innovative Technologies in Medicine and Dentistry, G. D'Annunzio University, Chieti, Italy.

Ebiomedicine
|October 9, 2022
PubMed

Insights

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection triggers the NLRP3 inflammasome, worsening COVID-19. Blocking interleukin-1 (IL-1) with anakinra improved survival in moderate-to-severe cases.

Area of Science:

  • Immunology
  • Virology
  • Pathophysiology

Background:

  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can lead to a hyperinflammatory response, worsening COVID-19 outcomes.
  • The SARS-CoV-2 interaction with angiotensin-converting enzyme 2 (ACE2) activates the NACHT, leucine-rich repeat, and pyrin domain-containing protein 3 (NLRP3) inflammasome.
  • Enhanced NLRP3 inflammasome activity correlates with increased COVID-19 severity and poorer prognosis.

Purpose of the Study:

  • To review the role of NLRP3 inflammasome and IL-1β in COVID-19 pathogenesis.
  • To discuss clinical trials investigating IL-1 inhibition for COVID-19 treatment.

Main Methods:

  • Review of current scientific literature on NLRP3 inflammasome activation in COVID-19.
  • Analysis of evidence linking inflammasome activity to disease severity, pulmonary injury, and hypercoagulability.
  • Summary of findings from clinical trials, including the SAVE-MORE trial, evaluating IL-1 blockers.

Main Results:

  • NLRP3 inflammasome activation and subsequent IL-1β release contribute to lung injury and hypercoagulability in COVID-19.
  • Observational studies and the SAVE-MORE trial demonstrated promising results with IL-1 blockers like anakinra.
  • Early anakinra treatment in the SAVE-MORE trial significantly reduced hospital stay and improved survival in moderate-to-severe COVID-19 patients.

Conclusions:

  • The NLRP3 inflammasome and IL-1β play a significant pathogenetic role in severe COVID-19.
  • Targeting IL-1 signaling represents a promising therapeutic strategy for managing moderate-to-severe COVID-19.
Keywords:
AnakinraC-reactive proteinCOVID-19CanakinumabColchicineIL-18IL-1βNLRP3 inflammasomeSARS-CoV-2

More Related Videos

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages06:52

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages

Published on: May 21, 2018

10.8K
Accurate and Simple Measurement of the Pro-inflammatory Cytokine IL-1β using a Whole Blood Stimulation Assay06:29

Accurate and Simple Measurement of the Pro-inflammatory Cytokine IL-1β using a Whole Blood Stimulation Assay

Published on: March 1, 2011

26.5K

Related Concept Videos

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
7.8K
T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
1.3K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
9.1K