Monocyte Priming Dysfunction
Monocyte Priming Dysfunction - Related Videos
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...
03:05
In Vitro Culture and Differentiation of Primary Monocytes into Macrophages
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2025
This video demonstrates the priming of primary monocytes into macrophages. Primary human monocytes can be isolated and differentiated to an M1-like pro-inflammatory phenotype using the granulocyte-macrophage colony-stimulating factor (GM-CSF) or to an M2-like anti-inflammatory phenotype using the macrophage colony-stimulating factor (M-CSF).
13:54
Tractable Mammalian Cell Infections with Protozoan-primed Bacteria
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Cited by 2 •
2013
This technique provides a method to harvest, normalize and quantify intracellular growth of bacterial pathogens that are pre-cultivated in natural protozoan host cells prior to infections of mammalian cells. This method can be modified to accommodate a wide variety of host cells for the priming stage as well as target cell types.
12:08
Tracking Mouse Bone Marrow Monocytes In Vivo
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Cited by 6 •
2015
Monocytes are key regulators of innate immunity and play a critical role in the renewal of the peripheral mononuclear phagocytic system and in case of inflammation. This manuscript describes the procedure of real time imaging of the mouse calvaria bone marrow to study the monocyte mobilisation mechanism.
08:31
Characterization of Human Monocyte-derived Dendritic Cells by Imaging Flow Cytometry: A Comparison between Two Monocyte Isolation Protocols
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Cited by 19 •
2016
This study compares two different methods of human monocyte isolation for obtaining in vitro dendritic cells (DCs). Monocytes are selected by adherence or negatively enriched by magnetic separation. Monocyte yield and viability along with MDDC viability, proliferation and CD11c/CD14 surface marker expression will be compared between both methods.
FAQs
Prior exposure changes how monocytes respond to a later challenge. Microbial products, cytokines, and tissue-injury signals can place these cells into a heightened-response state, but repeated or intense activation can instead reduce later inflammatory output. The key experimental question is therefore not simply whether monocytes are activated, but how their response has been reshaped by earlier signals.
Priming and tolerance represent opposite response patterns, but both arise from altered prior stimulation. Priming can amplify the response to a subsequent signal, whereas tolerance can suppress inflammatory mediator production after repeated or intense activation. Distinguishing these states matters because an amplified response may sustain harmful inflammation, while reduced responsiveness may weaken coordinated defense against infection.
These three layers help explain why altered responsiveness can persist beyond the initial exposure. Changes in signaling affect how incoming stimuli are interpreted, chromatin accessibility influences which inflammatory programs can be engaged, and metabolic changes support a different cellular response state. Considering them together connects immediate mediator release with longer-lasting immune dysregulation.
Reduced production of tumor necrosis factor during a tolerant state may impair aspects of pathogen control, while dysregulated activation can continue to support harmful inflammation. This apparent contradiction is central to the disorder: the same immune system can become less effective against microbes yet remain capable of damaging inflammatory activity, depending on the response state and stimulus history.
Researchers can compare monocyte responses after different prior exposures, including microbial products, cytokines, or tissue-injury signals, and then examine the response to a subsequent stimulus. Measuring changes in inflammatory mediators such as tumor necrosis factor helps distinguish heightened responsiveness from reduced output. This comparison links exposure history to functional immune consequences without treating all activation states as equivalent.
In sepsis research, the topic provides a framework for examining how intense or repeated immune stimulation may alter later monocyte behavior. Investigators can ask whether cells show excessive inflammatory activity, reduced mediator production, or a combination across response states. These patterns may help explain why infection can coexist with persistent inflammation and inadequate pathogen control.
Characterizing response states may support immune-monitoring biomarkers that indicate how monocytes have been functionally reshaped by prior signals. That information could also guide targeted therapies designed to address the relevant imbalance rather than broadly increasing or suppressing immunity. The same research logic applies to chronic infection and inflammatory disease, where defense failure and harmful inflammation may overlap.