Neutrophil Priming
Neutrophil Priming - Related Videos
09:34
Intravital Imaging of Neutrophil Priming Using IL-1β Promoter-driven DsRed Reporter Mice
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Cited by 1 •
2016
This current protocol employs fluorescent reporters, in vivo labeling, and intravital imaging techniques to enable monitoring of the dynamic process of neutrophil priming in living animals.
06:16
Verbal Priming
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2023
Source: Laboratory of Jonathan Flombaum—Johns Hopkins University Human memory seems to work in two broad ways. Like modern computers, the human mind has explicit, or declarative, memory: ask a question, and a person gives the best answer they can. Input a query, and a computer program returns the contents of the relevant parts of its stored memory. Humans also have a second kind of memory system, one not really typical of computers, one that experimental psychologists call implicit. Implicit...
04:00
A Murine Model of Primed Mycobacterial Uveitis to Study Post-Infectious Uveitis
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2025
This video demonstrates a method to generate a mouse model of primed mycobacterial uveitis (PMU) for studying post-infectious uveitis. Upon induction of PMU by intravitreal injection of heat-killed Mycobacterium tuberculosis in a mouse previously immunized with the same immunogen, the progression of chronic inflammation in the eye is analyzed using imaging and histopathological...
04:32
Induction and Visualization of Neutrophil Extracellular Traps in Pre-Labeled Neutrophils
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2025
This video demonstrates the induction and visualization of neutrophil extracellular traps or NETs in pre-labeled neutrophils using patient serum containing anti-neutrophil cytoplasmic antibodies. Furthermore, using an impermeable DNA dye and fluorescence microscopy enables the visualization of NETs.
07:12
Neutrophil Isolation Protocol
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Cited by 173 •
2008
Neutrophils are among the first cells to arrive on the site of inflammatory immune response, and their functions and mechanisms have been studied extensively in vitro. We demonstrate a standard density gradient separation method to isolate human neutrophils from whole blood using commercially available separation media.
FAQs
Priming alters receptor signaling so that neutrophils are prepared to respond more strongly when they encounter a subsequent activating signal. This preparation can enhance adhesion, migration, reactive oxygen species production, degranulation, and extracellular trap formation without requiring antimicrobial contents to be released during the initial priming state. The result is a faster and more effective response at sites of infection.
Cytokines, chemokines, and complement fragments can initiate neutrophil priming during infection or inflammation. These mediators act by changing receptor signaling rather than simply triggering immediate full activation. Their effects prepare the cells for later antimicrobial functions, allowing inflammatory signals to connect local tissue conditions with neutrophil recruitment and activity during microbial invasion.
Reversibility allows neutrophils to become more responsive temporarily without committing immediately to full antimicrobial release. This supports rapid host defense when infection is present while limiting unnecessary activation when conditions change. If priming becomes excessive or prolonged, however, the same enhanced responsiveness can intensify tissue injury and contribute to inflammatory disease.
The primed state can enhance several coordinated neutrophil functions, including adhesion to relevant sites, migration toward inflammation, reactive oxygen species production, degranulation, and extracellular trap formation. These outcomes represent different stages or forms of antimicrobial activity, from reaching the affected tissue to deploying mechanisms that can help control invading microbes.
In infection research, priming helps explain how neutrophils rapidly increase antimicrobial activity after exposure to inflammatory mediators. In sepsis, the concept is also important because excessive or prolonged priming may amplify inflammatory injury rather than improve pathogen control. Studying this balance can clarify how protective innate responses become harmful during severe systemic inflammation.
Researchers can examine whether inflammatory conditions increase neutrophil adhesion, migration, reactive oxygen species production, degranulation, or extracellular trap formation. Comparing these responses with the degree and duration of exposure to priming mediators can help distinguish beneficial preparation from potentially damaging overactivation. Such measurements are relevant to host defense, chronic inflammation, and immunomodulatory therapy research.