Page 136 - Veterinary Immunology, 10th Edition

VetBooks.ir Emigration From the Bloodstream

Neutrophils in the bloodstream are simply carried along by the
flow. In inflamed tissues, however, these fast-moving cells slow

down, stop, bind to blood vessel walls, and emigrate into the
tissues. This emigration is triggered by changes in the endothelial
cells that line blood vessel walls.

Changes in Endothelial Cells

In aggregate, the endothelial cells that line blood vessels collectively
have a huge surface area (estimated at 4000 square meters in
humans) and thus serve as a broad sensor of microbial invasion.
When PAMPs and DAMPs such as lipopolysaccharides or

histamine and platelet activating factor (PAF) from damaged
tissues reach blood vessels, they stimulate the endothelial cells to
express a sticky glycoprotein called P-selectin (CD62P). P-selectin is
stored in cytoplasmic granules but moves to the cell surface within

minutes after stimulation. The P-selectin can bind a protein called
L-selectin (CD62L) on passing neutrophils. At first, this binding is
weak and transient because the neutrophils shed their L-selectin,
but these neutrophils express more selectins so that they gradually

slow, roll along the endothelial cell surface, and eventually stop
(Fig. 5.6). This mainly happens in venules where the vessel wall is
thin and its diameter sufficiently small to permit the neutrophils to
make firm contact with the endothelium.

FIG. 5.6 The stages of neutrophil adhesion and emigration from

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