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Related Concept Videos

Caspases01:24

Caspases

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Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
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Factors Affecting the Risk of Infection01:26

Factors Affecting the Risk of Infection

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The hosts' susceptibility to infection depends on several factors. The integrity of the skin and mucous membranes helps protect the body against microbial attacks. When the skin is altered, the chance of infection, limb loss, and even death increases.
The integrity and count of the white blood cells help the body resist pathogens and fight infection. When impaired, it reduces the body's resistance to pathogens. The acidic pH levels of the gastrointestinal, genitourinary tracts, and skin...
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Myocarditis I: Introduction01:21

Myocarditis I: Introduction

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Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
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Inflammation01:38

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The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

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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...
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Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

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The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
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Related Experiment Video

Updated: Oct 26, 2025

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

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Do inflammasome impact COVID-19 severity?

Maria Beatriz Calado1, Crislayne Emilly da Silva Santana2, Sergio Crovella3

  • 1Laboratory of Immunopathology Keizo Asami, Recife, Brazil.

Virusdisease
|August 2, 2021
PubMed
Summary

The COVID-19 pandemic causes severe organ damage and inflammation, potentially driven by the NLRP3 inflammasome. Understanding this mechanism is crucial for addressing critical illness and fatality in SARS-CoV-2 infections.

Keywords:
ARDSCoagulationIL-1bInflammationNLRP3SARS-CoV-2

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

  • Immunology
  • Pathophysiology
  • Virology

Background:

  • The COVID-19 pandemic presents diverse clinical challenges, including severe complications in critical patients.
  • Extrapulmonary manifestations in organs like the heart and kidney are linked to poor outcomes.
  • A deregulated immune response and systemic inflammation are implicated in COVID-19 pathophysiology.

Purpose of the Study:

  • To review the role of the NLRP3 inflammasome in COVID-19.
  • To elucidate the mechanisms linking SARS-CoV-2 infection to organ injury and fatality.

Main Methods:

  • Literature review of clinical and scientific publications on COVID-19.
  • Analysis of the proposed involvement of the NLRP3 inflammasome in SARS-CoV-2 pathogenesis.

Main Results:

  • COVID-19 patients exhibit coagulopathies and microthrombi, contributing to complications.
  • The NLRP3 inflammasome is highlighted as a potential key player in the immune imbalance seen in severe COVID-19.
  • Extrapulmonary organ damage, particularly in the heart and kidney, is a significant factor in disease severity.

Conclusions:

  • The NLRP3 inflammasome appears to be directly involved in the clinical presentation of SARS-CoV-2 infection.
  • Further research is needed to fully understand the drivers of COVID-19-related organ injuries and systemic inflammation.
  • Targeting the NLRP3 inflammasome may offer therapeutic potential for severe COVID-19.