Abstract
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.
Graphical Abstract
Cardiovascular & Hematological Disorders-Drug Targets
Title:Neutrophil Migration Under Normal and Sepsis Conditions
Volume: 15 Issue: 1
Author(s): Yelena V. Lerman and Minsoo Kim
Affiliation:
Keywords: Cell adhesion, cell migration, cytokine, chemokine, endothelial cell, neutrophil, sepsis.
Abstract: 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.
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Cite this article as:
Lerman V. Yelena and Kim Minsoo, Neutrophil Migration Under Normal and Sepsis Conditions, Cardiovascular & Hematological Disorders-Drug Targets 2015; 15 (1) . https://dx.doi.org/10.2174/1871529X15666150108113236
DOI https://dx.doi.org/10.2174/1871529X15666150108113236 |
Print ISSN 1871-529X |
Publisher Name Bentham Science Publisher |
Online ISSN 2212-4063 |

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