Neutrophil Depletion
Neutrophil Depletion - Related Videos
06:17
Depletion of Specific Cell Populations by Complement Depletion
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Cited by 15 •
2010
To effectively study the function of immune cell populations their purification is often required. Complement depletion is a fast and inexpensive technique for the isolation of immune cell populations with high purity.
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.
08:50
Depletion and Reconstitution of Macrophages in Mice
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Cited by 118 •
2012
Macrophages play a central role in homeostasis and pathology in many tissues. The protocol presented here describes methods for depleting macrophages in vivo, deriving polarized macrophages from bone marrow aspirates, and adoptively transferring macrophages into mice. These techniques allow determination of the role that polarized macrophages play in health and disease.
11:07
Macrophage Cholesterol Depletion and Its Effect on the Phagocytosis of Cryptococcus neoformans
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Cited by 22 •
2014
In this article, a protocol for infection of macrophages with Cryptococcus neoformans is described. Also, a method for sterol depletion from the macrophages is explained. These protocols provide a guide to study fungal infections in vitro and examine the role of sterols in such infections.
FAQs
Neutrophil depletion can alter neutrophil availability in two conceptually different ways: targeting antibodies may promote clearance, whereas other selective approaches may block availability without relying on the same mechanism. This distinction matters because the observed phenotype may reflect fewer neutrophils, impaired participation, or both. Interpreting results therefore requires linking the intervention’s action to the immune response being measured.
Efficiency determines how strongly neutrophil-dependent functions are reduced, while specificity determines whether the result can be attributed to neutrophil loss rather than broader immune disruption. An incomplete reduction may underestimate neutrophil contributions, whereas unintended effects on overall immune function can complicate interpretation. Both factors are therefore essential when connecting an experimental outcome to neutrophil activity.
By reducing neutrophil availability while examining the resulting inflammatory or host-defense response, investigators can assess which effects depend on these cells. This approach is especially useful when several immune populations respond to the same infection, injury, or disease process. Comparisons with conditions lacking depletion help separate neutrophil-associated changes from effects mediated by other immune cells.
Researchers should establish that the intervention achieves the intended reduction, acts with appropriate specificity, and does not produce unrecognized changes in overall immune function. These checks are important because an apparent change in inflammation, infection outcome, or tissue repair could otherwise result from inefficient targeting or broader immune effects rather than from reduced neutrophil participation.
The strategy is applied in infection models to examine neutrophil contributions to host defense and in autoimmune studies to investigate their role in inflammation. Cancer research also uses it to assess neutrophil-associated effects in disease settings. Across these applications, the approach helps determine whether a biological outcome depends on neutrophils or persists through mechanisms involving other immune cells.
Reduced neutrophil availability can increase susceptibility to infection and alter tissue repair, reflecting the cells’ contribution to rapid responses against invading microbes and injury. It can also change inflammatory outcomes in disease models. These consequences make depletion both informative and potentially confounding, so researchers must consider altered host defense and repair when evaluating experimental results.