Related Experiment Video

Updated: Feb 25, 2026

Visualization of Inflammatory Caspases Induced Proximity in Human Monocyte-Derived Macrophages
08:41

Visualization of Inflammatory Caspases Induced Proximity in Human Monocyte-Derived Macrophages

Published on: April 6, 2022

3.2K

Lysophosphatidylcholine activates caspase-1 in microglia via a novel pathway involving two inflammasomes

Holger Scholz1, Claudia Eder1

  • 1Charité - Universitätsmedizin Berlin, Institute of Physiology, 10117 Berlin, Germany.

Journal of Neuroimmunology
|August 6, 2017
PubMed

Insights

This study reveals that lysophosphatidylcholine (LPC) activates inflammasomes, leading to caspase-1 activation in microglia. Optimal activation requires both NLRP3 and NLRC4 inflammasomes, crucial for neuroinflammation.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Microglia are key immune cells in the brain.
  • Inflammasomes regulate inflammatory responses.
  • Neuroinflammation is implicated in brain pathology.

Purpose of the Study:

  • To identify inflammasomes involved in microglial caspase-1 activation induced by lysophosphatidylcholine (LPC).
  • To elucidate the signaling pathways mediating LPC-induced neuroinflammation.

Main Methods:

  • Microglial cell cultures were stimulated with LPC.
  • Lipopolysaccharide (LPS) prestimulation was employed.
  • Inflammasome components (NLRP3, ASC, NLRC4) were assessed using knockdown techniques.
  • Caspase-1 activation was measured.

Main Results:

  • LPC-induced caspase-1 activation in microglia was dependent on LPS prestimulation, NLRP3, and ASC.
  • Knockdown of NLRC4 also inhibited LPC-stimulated caspase-1 activity.
  • Optimal caspase-1 activation by LPC requires the involvement of both NLRP3 and NLRC4 inflammasomes.

Conclusions:

  • Lysophosphatidylcholine (LPC) triggers a dual inflammasome response in microglia.
  • NLRP3 and NLRC4 inflammasomes are essential for LPC-mediated caspase-1 activation.
  • This finding advances understanding of microglial inflammasome activation in neuroinflammation.
Keywords:
Caspase-1InflammasomeLysophospholipidsMicroglia

More Related Videos

Evaluation of Caspase Activation to Assess Innate Immune Cell Death10:23

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

3.9K
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

11.3K

Related Concept Videos

Caspases01:24

Caspases

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...
14.3K
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized...
5.3K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
9.0K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
8.8K
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
15.7K
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
8.6K