Pyroptosis
Pyroptosis - Related Videos
05:14
Examination of Pyroptosis by Flow Cytometry
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2024
This article describes the identification of pyroptotic cells using flow cytometry after dual staining with antibodies against the N-terminal fragment of chicken GSDME (chGSDME-NT) and propidium iodide (PI).
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.
03:02
A Lactate Dehydrogenase Release Assay To Detect Macrophage Death Following Nigericin Exposure
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2025
This video demonstrates the lactate dehydrogenase assay to detect inflammasome-mediated macrophage death. The macrophages are exposed to lipopolysaccharide for priming, followed by exposure to nigericin to cause inflammasome-induced cell death, which is determined by the lactate dehydrogenase assay.
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.
FAQs
Inflammasomes act as signaling platforms that respond to pathogen-associated or danger-associated signals. Their activation leads to activation of inflammatory caspases, which then cleave gasdermin proteins. This sequence connects detection of infection or cellular stress to membrane pore formation and the inflammatory consequences that follow within the affected cell.
After inflammatory caspases cleave gasdermin proteins, the resulting fragments form pores in the cell membrane. These pores disrupt the cell’s integrity, producing swelling and eventual rupture. They also enable the affected cell to release inflammatory cytokines, including interleukin-1β and interleukin-18, linking structural damage to immune signaling.
Pyroptosis can be beneficial when it destroys an intracellular pathogen’s cellular niche and releases cytokines such as interleukin-1β and interleukin-18. However, excessive activation may damage tissues and contribute to inflammatory disease. This balance makes pathway control important when interpreting whether the response is protective or harmful in a biological context.
A pathway study can trace the sequence from pathogen-associated or danger-associated signals to inflammasome activation, inflammatory caspase activity, gasdermin cleavage, pore formation, swelling, and rupture. Researchers can also examine cytokine release, particularly interleukin-1β and interleukin-18. Together, these events provide connected molecular and cellular outcomes for investigating infection and cellular stress.
In infection research, the pathway is relevant because destroying a cell can eliminate the intracellular niche used by pathogens, while cytokine release contributes to the inflammatory response. Cancer research also examines pyroptosis as part of broader efforts to understand regulated cell death and its possible therapeutic relevance, as indicated by the pathway’s connection to therapeutic strategies.
Therapeutic studies can ask whether immune-driven cell death should be enhanced, restrained, or otherwise modulated in a particular biological context. The rationale is that pyroptosis can help respond to infection, but excessive activation may damage tissues and contribute to inflammatory disease. This opposing potential gives pathway modulation relevance to infection, autoimmunity, cancer, and inflammation-focused research.