Leukocyte Adhesion
Leukocyte Adhesion - Related Videos
06:20
Imaging Leukocyte Adhesion to the Vascular Endothelium at High Intraluminal Pressure
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Cited by 22 •
2011
This is a method to visualise leukocyte adhesion to the endothelium in harvested pressurised vessels. The technique enables studying vascular adhesion under shear flow with differing intraluminal pressures up to 200 mmHg thus mimic-ing the pathophysiological conditions of high blood pressure.
05:12
Intravital Microscopy of Leukocyte-endothelial and Platelet-leukocyte Interactions in Mesenterial Veins in Mice
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Cited by 11 •
2015
This simplified application of intravital microscopy of mesentery veins in mice can be used in different models of inflammation to observe leukocyte-endothelial and platelet-leukocyte interactions.
10:16
Visualizing Leukocyte Rolling and Adhesion in Angiotensin II-Infused Mice: Techniques and Pitfalls
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Cited by 6 •
2018
This manuscript describes the use of transgenic reporter mice and different administration routes of fluorescent dyes in angiotensin II-induced hypertension using intravital video microscopy of blood vessels to evaluate the activation of immune cells and their ability to roll and adhere to the endothelium.
03:42
Isolation of Marginating Hepatic Leukocytes from a Mouse Liver
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2025
In this video, we demonstrate the isolation of marginating hepatic leukocytes from mouse liver by forced perfusion.
06:44
Isolation of Brain-infiltrating Leukocytes
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Cited by 33 •
2011
A rapid method to obtain infiltrating leukocytes from the murine brain is described. This method utilizes a continuous Percoll gradient and discontinuous Ficoll gradient to select and purify the leukocyte-enriched layer. Isolated leukocytes may then be characterized by flow cytometric measurements.
FAQs
Selectins support the initial, transient interactions that slow leukocytes and produce rolling along the endothelial surface. This stage does not create the stable attachment needed for tissue entry. Instead, it positions circulating cells where they can encounter endothelial chemokines and receive signals that prepare the next adhesion step, making rolling an essential transition between blood flow and directed recruitment.
Endothelial chemokines activate leukocyte integrins, changing the cells from a rolling state to one capable of strong binding. Activated integrins then attach to ligands on the endothelium and establish firm adhesion. This switch is important because it prevents the leukocyte from being carried away by blood flow and enables subsequent movement across the vascular barrier.
The sequence separates capture, activation, stable attachment, and tissue entry into functionally distinct steps. Selectin-dependent rolling provides time and contact for chemokine signaling, while integrin activation supplies the stronger interaction required for firm adhesion. Coordinating these stages allows inflammatory recruitment to respond to local endothelial signals instead of causing indiscriminate attachment throughout the circulation.
Inflammatory signals induce endothelial cells to display adhesion molecules that can interact with passing leukocytes. The resulting surface changes provide the molecular contacts needed for rolling and later firm binding. In vascular inflammation, this endothelial response therefore helps determine whether circulating immune cells remain in the bloodstream or become positioned for entry into affected tissue.
In nervous tissue, adhesion regulates how immune cells interact with the vessels that separate the circulation from neural environments. Changes in this process can influence immune-cell entry, blood-brain barrier function, and the intensity of neuroinflammation. Studying these connections helps researchers relate vascular behavior to inflammatory responses in the nervous system rather than viewing neural disease as purely neuronal.
The process provides a framework for examining how inflammatory signals, endothelial adhesion molecules, and leukocyte movement contribute to neurological damage or repair responses. Researchers can use this framework to connect vascular and immune mechanisms with disease-associated neuroinflammation. Because each adhesion stage offers a distinct control point, the pathway also helps identify potential therapeutic targets for modifying immune-cell recruitment.