Simplified overview of proposed neutrophil–endothelial interactions during ontogeny. Before E14 to E15, hemogenic endothelial activity predominates, whereas after this time, HSC and progenitor activity concentrates extravascularly within the fetal liver, followed by seeding of bone marrow. (1) Neutrophil egress to the vasculature from the fetal liver (E14-E15) or the bone marrow (after E18). (2) Neutrophil rolling on activated endothelium occurs under conditions of low shear stress and is mediated by adhesive mechanisms such as neutrophil P-selectin glycoprotein ligand 1 interacting with activated endothelial P-selectin. (3) Firm arrest/adhesion involves interactions between activated neutrophils that express surface adhesion molecules, including Mac-1 and lymphocyte function-associated antigen 1, and cognate endothelial ligands such as the ICAMs. (4) Transendothelial migration/extravasation. Activated neutrophils migrate through endothelial gap junctions using adhesive interactions that include CD18 and CD31. (5) Chemotaxis. Activated neutrophils migrate toward inflammatory tissue in a directed process mediated by chemokines such as interleukin 8. (6) Phagocytosis and bacterial killing. Activated tissue neutrophils ingest pathogens and promote their intracellular demise. (7) Apoptosis. Tissue neutrophils undergo programmed cell death in preparation for their removal by the reticuloendothelial system by efferocytosis (8).