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Inflammation is a rapid and complex reaction to an injurious agent that initiates a cascade of events which lead to vascular responses, neutrophil recruitment and activation, and multiple systemic reactions. The initiation of inflammation after an insult is exudation. Exudation is the localized hemodynamic changes that are critical to subsequent neutrophil emigration because selectin-mediated, low-affinity, endothelial adhesive interactions can only occur in the presence of shear forces exerted by hemoconcentration. A critical function of inflammation is to deliver neutrophils to the site of insult so the initiation of leukocyte activation can occur. The migration of neutrophils from the intravascular to extravascular space requires a…show more content…
All integrins are composed of two linked polypeptide chains, α and β. The β2 integrins are called CD11/CD18 where CD11 refers to the α chain and CD18 refers to the β2 subunit (Kumar et al, 2005). CD11/CD18 play a primary roll in adhesion of leukocytes to other cells which mediates leukocyte attachment and extravasation or transmigration. Binding of signaling molecules to surface receptors on the leukocytes activates them and triggers changes in the affinity of β2 integrins that are present on their plasma membranes. β2 integrins are recognized by counterligands on the endothelial cells. Following engagement of integrins, leukocytes tightly adheren using both integrins and selectins, become transiently arrested, undergo shape change, and migrate from the blood to the extravascular inflammatory environment. To complete the process of transmigration, neutrophils require chemoattractants to direct neutrophils to specific areas of inflammation to eliminate the offending agent. The importance of integrin-mediated adhesion to neutrophil delivery and host defense is demonstrated in patients with leukocyte adhesion deficiency type 1 (LAD-1). LAD syndromes result from the failure of innate host defences that result in defective adhesion and targeting of leukocytes to sites of microbial invasion. LAD-1 is an autosomal recessive immunodeficiency caused by mutations is the β2 integrin, CD18, which impairs CD11/CD18 surface expression. Absence of
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