Normal polymorphonuclear leukocyte (PMN) emigration from the vasculature to the site of infection in the tissues.
In response to an infection in the tissues, inflammatory signals (arrows) diffuse to the vasculature and activate the vascular endothelium causing release of chemokines (4-pointed stars), which attract PMNs to the endothelial surface. Attraction is followed by selectin-mediated PMN rolling and β2-integrin:ICAM-1 mediated firm adhesion of PMNs to endothelial cells (ECs).10 These PMNs, which have undergone a change from a non-adhesive to an adhesive phenotype are now primed.10,31 Priming of PMNs enhances the microbicidal function of PMNs to a subsequent stimulus and changes the activity of PMNs such that stimuli that normally do not cause activation of quiescent neutrophils are able to activate primed PMNs.10,31 It is important to note that priming is part of the orderly process of PMN transmigration to the tissues, and although there are benefits to enhanced PMN function including efficient destruction of pathogens, it is clear priming may be detrimental to the host leading to PMN-mediated organ injury, especially acute respiratory distress syndrome (ARDS).10,31 The PMNs then diapedese through the endothelial layer, chemotax to the site of infection and phagocytize and destroy the bacterial invaders.10
