Inflammation increases vascular permeability and recruits leukocytes through a sequence of interactions with the endothelium.
Formation of extravascular fluid
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An exudate forms during inflammation when endothelial cells retract, increasing vascular permeability and creating spaces through which fluid and proteins pass.
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A transudate forms when fluid escapes because hydrostatic pressure increases or osmotic pressure decreases.
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Normal capillary hydrostatic pressure falls from about 32 mm Hg at the arterial end to 12 mm Hg at the venous end. The source describes virtually no net fluid flow across the vascular bed in the steady state.
Sequence of leukocyte migration
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Leukocytes first roll along the endothelium, become activated, adhere firmly, and then transmigrate across the endothelium.
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After crossing the endothelium, leukocytes pierce the basement membrane and move toward chemoattractants released from the source of injury.
Molecules responsible for each step
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Selectins mediate rolling. E-selectin and P-selectin are expressed on endothelial cells, whereas L-selectin is expressed on leukocytes.
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Chemokines displayed on proteoglycans activate neutrophils and increase the avidity of their integrins.
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Integrins mediate firm adhesion. Intercellular adhesion molecule-1, abbreviated ICAM-1, is an integrin ligand.
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Platelet endothelial cell adhesion molecule-1, also called PECAM-1 or CD31, mediates transmigration.