Inflammasome Complex
Inflammasome Complex - Related Videos
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.
03:44
Detection of Inflammasome Activation via Fluorescence Microscopy
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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.
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.
08:42
Coordination Chemistry Complexes
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2023
Source: Laboratory of Dr. Neal Abrams — SUNY College of Environmental Science and Forestry Transition metals are found everywhere from vitamin supplements to electroplating baths. Transition metals also make up the pigments in many paints and compose all minerals. Typically, transition metals are found in the cationic form since they readily oxidize, or lose electrons, and are surrounded by electron donors called ligands. These ligands do not form ionic or covalent bonds with the metal center,...
02:41
Protein Complex Assembly
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2020
Proteins can form homomeric complexes with another unit of the same protein or heteromeric complexes with different types. Most protein complexes self-assemble spontaneously via ordered pathways, while some proteins need assembly factors that guide their proper assembly. Despite the crowded intracellular environment, proteins usually interact with their correct partners and form functional complexes. Many viruses self-assemble into a fully functional unit using the infected host cell to...
FAQs
Sensor choice shapes the upstream entry point of inflammasome signaling. NLRs and AIM2 are examples of sensor proteins that respond to cellular stress, microbial components, or infection-related signals and then recruit ASC. This distinction matters because studies can examine how different host-cell detection routes converge on the same downstream inflammatory machinery during infection.
ASC serves as the adaptor that connects an activated sensor to caspase-1. Once recruited, caspase-1 processes the precursor forms pro-interleukin-1β and pro-interleukin-18 into inflammatory mediators. Following this sequence helps researchers distinguish sensor activation from cytokine maturation and interpret where a defect or intervention acts within the pathway.
Pyroptotic cell death adds a cellular outcome to cytokine release. Caspase-1 activation can trigger this inflammatory form of cell death, so inflammasome studies may evaluate both processed interleukins and loss of viable host cells. Considering both outputs is important when assessing how innate responses restrict intracellular microbes or instead contribute to tissue damage.
An inflammasome-focused analysis can follow three linked outcomes: the initiating cellular stress, microbial component, or infection-related signal; recruitment of ASC and activation of caspase-1; and processing of pro-interleukin-1β and pro-interleukin-18. Researchers can then determine whether responses also include pyroptotic death, creating a pathway-based interpretation rather than relying on one endpoint.
It connects microbial or infection-related detection with innate immune outputs. This framework allows infection studies to ask how host cells recognize pathogens, coordinate inflammation, and restrict intracellular microbes. It also provides a way to compare responses in which cytokine processing occurs with those that additionally involve pyroptotic cell death, clarifying how cellular and inflammatory outcomes are linked.
Beyond infection models, inflammasome research is relevant when inflammation becomes maladaptive. Dysregulated activity can be associated with autoinflammatory disease, tissue damage, or chronic infection. Examining sensors, ASC, caspase-1, and cytokine processing helps connect a molecular pathway to disease mechanisms and identifies inflammasome components as potential targets for studying anti-inflammatory therapies.