Neutrophil Adhesion
Neutrophil Adhesion - Related Videos
12:42
Human Neutrophil Flow Chamber Adhesion Assay
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Cited by 12 •
2014
A method of quantitating neutrophil adhesion is reported. This method creates a dynamic flow environment similar to that encountered in a blood vessel. It allows the investigation of neutrophil adhesion to either purified adhesion molecules (ligand) or endothelial cell substrate (HUVEC) in a context similar to the in vivo environment with sheer stress.
04:25
In Vitro Adhesion Assay to Detect the Adherence of Cancer Cells to Neutrophil Extracellular Traps
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2025
In this video, we demonstrate an assay utilizing fluorescence microscopy to detect the adhesion of cancer cells to neutrophil extracellular traps (NETs). In the test wells, there is a notable increase in the number of fluorescently labeled cancer cells adhering to NETs, whereas wells treated with DNase exhibit reduced cancer cell adhesion to NETs.
03:15
Fluorescence Microscopy of Neutrophil Extracellular Traps or NETs: A Technique to Observe Adhesive Interaction Between Cancer Cells and NETs
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2023
This video demonstrates the fluorescent staining of neutrophil extracellular traps (NETs), the extracellular DNA components expelled by neutrophils. This technique enables the visualization of adhesive interaction between cancer cells and NETs.
11:22
Quantitative In vitro Assay to Measure Neutrophil Adhesion to Activated Primary Human Microvascular Endothelial Cells under Static Conditions
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Cited by 29 •
2013
Neutrophil adherence to the activated endothelium at sites of infection is an integral component of the host's inflammatory response. Described in this report is a neutrophil binding assay that allows for the in vitro quantitation of primary human neutrophil binding to endothelial cells activated by inflammatory mediators under static conditions.
03:05
Time-lapse Fluorescence Microscopy of Neutrophil Extracellular Traps or NETs: A Technique to Analyze Post-adhesion Interaction between Cancer Cells and NETs
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2023
In this video, we analyze the post-adhesion behavior of cancer cells trapped in neutrophil extracellular traps (NETs) by co-culturing low-density neutrophils and gastric cancer cells. The time-lapse video analysis helps monitor various cellular events and study the role of NETs in pathological conditions.
FAQs
They perform different functions during recruitment. Endothelial selectins first support transient interactions that slow neutrophils and promote rolling along the vessel wall. Chemokine signaling then activates neutrophil integrins, allowing β2 integrins to bind firmly to endothelial molecules such as ICAM-1. This progression coordinates initial contact with stable attachment before movement through the vessel wall.
Chemokines provide the activating signal that changes neutrophil integrins from an insufficiently adhesive state to one capable of firm binding. After this activation, β2 integrins can interact with endothelial ICAM-1 rather than supporting only transient contact. This step links inflammatory signaling to physical retention at the vessel wall, positioning neutrophils for subsequent transmigration.
The sequence creates a controlled route from circulation to affected tissue. Rolling allows neutrophils to interact with the endothelium, firm binding stabilizes their position, and transmigration carries them through the vessel wall. Once outside the vessel, they can move toward microbial or tissue-derived signals, connecting vascular recruitment with localized innate immune defense.
Infection and tissue injury are the principal conditions identified in this process. Inflammatory signals generated in these settings prompt endothelial cells to display selectins and support chemokine-dependent integrin activation on neutrophils. The resulting adhesion and tissue entry help direct innate immune cells toward locations where microbial threats or tissue damage require a response.
A useful analysis follows the linked stages of endothelial selectin display, neutrophil rolling, chemokine-driven integrin activation, firm binding to adhesion molecules such as ICAM-1, and transmigration through the vessel wall. Examining these stages separately helps identify whether a recruitment problem arises during initial contact, stable attachment, or passage into tissue.
These studies can clarify how leukocytes are recruited during inflammatory defense and how neutrophils reach affected tissues. They also help distinguish consequences of insufficient trafficking from those of excessive recruitment. That distinction is relevant to disorders in which impaired neutrophil movement may weaken defense, whereas excessive trafficking may contribute to inflammatory disease.