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 cells which is mediated by adhesion molecules called integrins. Integrins are proteins that promote cell-cell interaction. 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 functional CD11/CD18 integrins on leukocytes, leads to their incapacity to adhere to the endothelium and migrate to sites of infection. These patients develop recurrent or unresolved localized infection, impaired wound healing, and systemic sepsis because leukocytes are unable to undergo transmigration to sites of inflammation as a result of a genetic mutation on CD18 (Bunting, Harris, McIntyre, Prescott, & Zimmerman, 2002).

Bunting, M., Harris, E., McIntyre, T., Prescott, S., & Zimmerman, G. (2002). Leukocyte adhesion deficiency syndromes: adhesion and tethering defects involving β2 integrins and selectin ligands. Current Opinion in Hematology, Vol. 9; pp. 30+. Retrieved October 05, 2007, from Google Scholar. http://www.co-hematology.com/pt/re/cohematology/fulltext.00062752-200201000- Kumar, V., Abbas, A., & Fausto, N. (2005) Pathologic Basis of Disease. Philadelphia: Elsevier Saunders.

Seely, A., Pascual, J, & Christou, N. (2003). Science review: Cell membrane expression (connectivity) regulates Neutrophil delivery, function, and clearance. Critical Care, Vol. 7; pp. 291+. Retrieved October 03, 2007, from CINAHL Plus with Full Text.