Neutrophil migration is critical for pathogen clearance and host survival during severe sepsis.
Interaction of neutrophil adhesion receptors with ligands on endothelial cells results in firm adhesion of the
circulating neutrophils, followed by neutrophil activation and directed migration to sites of infection
through the basement membrane and interstitial extracellular matrix. Proteolytic enzymes and reactive
oxygen species are produced and released by neutrophils in response to a variety of inflammatory stimuli.
Although these mediators are important for host defense, they also promote tissue damage. Excessive neutrophil migration
during the early stages of sepsis may lead to an exaggerated inflammatory response with associated tissue damage and
subsequent organ dysfunction. On the other hand, dysregulation of migration and insufficient migratory response that
occurs during the latter stages of severe sepsis contributes to neutrophils’ inability to contain and control infection and
impaired wound healing. This review discusses the major steps and associated molecules involved in the balance of
neutrophil trafficking, the precise regulation of which during sepsis spells life or death for the host.
Keywords: Cell adhesion, cell migration, cytokine, chemokine, endothelial cell, neutrophil, sepsis.
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