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Adhesive glycoproteins on both neutrophils and vascular endothelial cells are known to mediate adhesive interaction between the two cell types. We propose that activation of endothelial cells will lead to the capture of unactivated neutrophils, localizing them at inflammatory sites. The interaction between activated endothelium and captured neutrophils will result in the stimulation of adherent neutrophils. Adherent activated neutrophils are then able to recruit incoming unactivated neutrophils by capturing them, further increasing the number of neutrophils at the inflammatory site. The formation of an adherent neutrophil aggregate will reduce plasma leakage from the vasculature as neutrophils migrate into tissue and will protect migrating neutrophils from shear stress of blood flow.