regulation of neutrophil extravasation

Definition

Target type: biologicalprocess

Any process that modulates the frequency, rate or extent of neutrophil extravasation. [GOC:mah]

Neutrophil extravasation, the process by which neutrophils exit the bloodstream and migrate to sites of inflammation, is a tightly regulated cascade of events involving adhesion molecules, chemoattractants, and signaling pathways. It can be summarized in four main steps:

1. **Rolling:** Neutrophils initially interact with the vascular endothelium through weak, transient interactions with selectin molecules, such as E-selectin and P-selectin. This interaction allows neutrophils to slow down and "roll" along the endothelium.

2. **Activation and Tight Adhesion:** As neutrophils encounter chemokines, such as IL-8 and CXCL1, they become activated and express integrins like LFA-1 and Mac-1. These integrins bind to their ligands, ICAM-1 and ICAM-2, on the endothelium, leading to firm adhesion of neutrophils to the vascular wall.

3. **Diapedesis:** Adhered neutrophils then migrate through the endothelial junctions, a process known as diapedesis. This involves complex interactions between the neutrophil cytoskeleton, adhesion molecules, and the endothelial cell junctions.

4. **Migration:** Once in the tissue, neutrophils follow chemoattractant gradients, such as those created by bacterial products or chemokines, to reach the site of inflammation. This movement involves the coordinated action of the neutrophil cytoskeleton and signaling pathways.

The regulation of neutrophil extravasation is essential for controlling inflammation. Dysregulation of this process can contribute to both excessive and insufficient inflammatory responses, leading to various pathological conditions. For example, impaired neutrophil extravasation can result in increased susceptibility to infections, while excessive extravasation can lead to tissue damage in conditions like sepsis or autoimmune diseases.'
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Proteins (1)

Compounds (11)