Selectins in leukocyte rolling and fluid accumulation mechanisms
THE CONTEXT
Selectins mediate early leukocyte attachment to endothelium. The accompanying fluid-formation material contrasts transudates with inflammatory exudates.
Selectin function and distribution
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Selectins mediate the initial weak binding of leukocytes and their rolling on endothelium.
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Selectins have an extracellular carbohydrate-binding domain. Their ligands are sialic acid-containing oligosaccharides attached to glycoprotein backbones on leukocytes or endothelial cells.
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Endothelial cells express E-selectin, P-selectin, and the ligand for L-selectin. Leukocytes express L-selectin.
Restriction to inflammatory sites
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E-selectin and P-selectin are absent or expressed at low levels on nonactivated endothelium. Cytokines and other mediators increase their expression, largely restricting leukocyte binding to sites of infection or tissue injury.
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In nonactivated endothelial cells, P-selectin is primarily stored in membrane-bound Weibel-Palade bodies.
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Within minutes of exposure to histamine or thrombin, P-selectin moves to the endothelial cell surface.
Fluid formation
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Transudates have low protein content and few cells. Increased hydrostatic pressure can result from venous outflow obstruction, as in congestive heart failure.
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Decreased colloid osmotic pressure can accompany decreased protein synthesis in liver disease, increased protein loss in kidney disease, or protein malnutrition such as kwashiorkor.
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Inflammatory exudates have high protein content and may contain white and red blood cells. Opening of interendothelial spaces permits fluid and protein leakage.