Acute inflammatory vascular changes and leukocyte recruitment
THE CONTEXT
Inflammation changes vascular flow and permeability and recruits circulating leukocytes into affected tissues through a sequence of endothelial interactions.
Vascular and lymphatic reactions
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Chemical mediators induce vasodilation, causing erythema and stasis of blood flow.
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Histamine, kinins, and other mediators increase vascular permeability by producing gaps between endothelial cells. Direct or leukocyte-induced endothelial injury can also increase permeability.
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Increased permeability permits plasma proteins and leukocytes involved in host defense to enter sites of infection or tissue damage.
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Fluid leakage from vessels, termed exudation, produces edema.
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Inflammation may cause redness of lymphatic vessels and swelling of lymph nodes.
Recruitment sequence and mediators
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Leukocytes move from blood into extravascular tissue containing pathogens or damaged tissue and become activated to perform defensive functions.
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Selectins mediate loose attachment and rolling on endothelium. Integrins mediate firm attachment, followed by migration through interendothelial spaces.
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TNF and IL-1 promote endothelial expression of selectins and integrin ligands.
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Chemokines increase integrin avidity for ligands and direct leukocyte migration.
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Tissue macrophages and other cells responding to pathogens or tissue damage produce many of these cytokines.
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Neutrophils predominate early and are later replaced by monocytes, which differentiate into tissue macrophages.
Keloid appearance
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Keloids may appear erythematous in light skin tones or hyperpigmented in darker skin.
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Microscopy shows thick connective tissue deposited in the dermis.