Non-canonical Inflammasome
Non-canonical Inflammasome - Related Videos
03:44
Detection of Inflammasome Activation via Fluorescence Microscopy
0 Views •
2025
This video demonstrates a method to detect NLRP3 inflammasome activation in macrophages using fluorescent reporter probes. The cells are treated with potassium ionophores and glycine to induce inflammasome assembly and caspase-1 activation. Fluorescent reporter probes visualize activated caspase-1, and cells are stained with a fluorescent dye for nuclei visualization.
03:06
An In Vitro Technique to Study Inflammasome Complex Formation in Macrophages
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2025
This video demonstrates a technique to study NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome formation in primary macrophages via immunofluorescence. The macrophages are first primed with bacterial lipopolysaccharide (LPS) to upregulate NLRP3 protein expression. Exposing the macrophages to nigericin—a potassium ionophore—leads to the activation of NLRP3 and the formation of inflammasomes, which are visualized via immunofluorescence.
09:04
Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
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Cited by 7 •
2014
Dendritic cells (DCs) secrete IL-1β in response to TLR8 recognition of synthetic purine, R848, followed by NLRP3 inflammasome activation with nigericin, therefore, IL-1β can be used to measure NLRP3 inflammasome activity. Intracellular cytokine staining, immunoblotting, and ELISA are used to accurately measure NLRP3 inflammasome priming and activation via IL-1β expression.
01:41
Non-Canonical Wnt Signaling Pathways
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2023
Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
01:41
Non-Canonical Wnt Signaling Pathways
0 Views •
2023
Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
FAQs
The initiating sensor differs by species: human cells use caspases-4 and -5, whereas mouse cells use caspase-11. These inflammatory caspases recognize cytosolic LPS and then cleave gasdermin D. This distinction is important when interpreting experiments or translating findings between human and mouse models, because the corresponding caspase components are not identical.
Gasdermin D provides the direct link between inflammatory caspase activation and membrane damage. After cleavage, it forms pores in the cell membrane, producing the structural change associated with pyroptosis. This event can cause cell death and release inflammatory signals, so gasdermin D functions as a central effector rather than merely an upstream sensor of bacterial material.
Potassium efflux connects the initial cytosolic LPS response to activation of the NLRP3 inflammasome. This secondary step expands the inflammatory output beyond pore formation and pyroptotic death by promoting maturation of interleukin-1β and interleukin-18. Consequently, the pathway can combine rapid cellular disruption with production of mature inflammatory cytokines.
Engagement can be understood through a sequence of linked outcomes: inflammatory caspase activity, gasdermin D cleavage, membrane pore formation, pyroptotic cell death, potassium efflux, and NLRP3-dependent cytokine maturation. Considering these events together helps distinguish the initial cytosolic LPS response from its downstream consequences, including release of inflammatory signals and mature interleukin-1β or interleukin-18.
Gram-negative bacterial infection can place LPS inside the cytosol, where it is detected by the species-specific inflammatory caspases described above. Subsequent gasdermin D pore formation and pyroptotic death help generate an inflammatory response to the infection. Studying this sequence clarifies how intracellular sensing of a bacterial component contributes to host defense.
The same signaling events that support protection against infection can also produce excessive inflammation when poorly controlled. Because the pathway drives pyroptotic death, inflammatory signal release, and maturation of interleukin-1β and interleukin-18, it provides a framework for investigating sepsis and autoinflammatory disease. It also supports research into strategies designed to regulate excessive inflammatory responses.