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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 multi-step combination of mechanical, chemical, and molecular processes. The first step is ‘margination’ or the movement of neutrophils from the center of venules to the periphery of the endothelium. This movement results from erythrocyte-leukocyte interactions that are caused by hemodynamic changes in the vessel.
A weak adhesive interaction between the leukocyte and endothelial cell allows the leukocyte to “roll” along the endothelial cell surface of the venule. The interaction involved in rolling is primarily governed by glycoprotein surface adhesion molecules called selectins (Seely, Pascual, & Christou, 2003). Selectins function to adhere leukocytes to endothelial cells. The binding of selectins to their ligands occurs rapidly with a low-affinity which allows selectins to mediate initial attachment and rolling of leukocytes on endothelial cells in the face of flowing blood (Kumar, Abbas, & Fausto, 2005).
Rolling, mediated by a weak molecular interaction, is a pre-requisite that allows the strong molecular interaction of adherence to occur. Adherence is a stationary adhesive interaction between leukocytes and endothelial…...

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