Abstract
Sepsis and septic shock continue to be a major cause of morbidity and mortality in critically ill patients. During the onset of sepsis, several inflammatory mediators, including cytokines, chemokines and nitric oxide are released systemically and mediate most of the pathophysiological events present in sepsis and septic shock, such as cardiovascular dysfunction and target-organ lesions. Polymorphonuclear leukocytes are critical effector cells during the inflammatory process and their migration to the infection focus is extremely important for the local control of bacterial growth and consequently for the prevention of bacterial dissemination. In experimental models and in human sepsis a profound failure of neutrophil migration to the infection focus is observed. It seems that the failure of neutrophil migration is dependent on toll-like receptor 4 (TLR4) and mediated by cytokines and chemokines, which induce the production of nitric oxide that inhibits neutrophil adhesion to venular endothelium and also the neutrophil chemotactic ability.
Keywords: Sepsis, polymorphonuclear neutrophil, neutrophil migration, adhesion, nitric oxide, cytokine
Endocrine, Metabolic & Immune Disorders - Drug Targets
Title: Neutrophil Function in Severe Sepsis
Volume: 6 Issue: 2
Author(s): J. C. Alves-Filho, B. M. Tavares-Murta, C. Barja-Fidalgo, C. F. Benjamim, A. Basile-Filho, S. M. Arraes and F. Q. Cunha
Affiliation:
Keywords: Sepsis, polymorphonuclear neutrophil, neutrophil migration, adhesion, nitric oxide, cytokine
Abstract: Sepsis and septic shock continue to be a major cause of morbidity and mortality in critically ill patients. During the onset of sepsis, several inflammatory mediators, including cytokines, chemokines and nitric oxide are released systemically and mediate most of the pathophysiological events present in sepsis and septic shock, such as cardiovascular dysfunction and target-organ lesions. Polymorphonuclear leukocytes are critical effector cells during the inflammatory process and their migration to the infection focus is extremely important for the local control of bacterial growth and consequently for the prevention of bacterial dissemination. In experimental models and in human sepsis a profound failure of neutrophil migration to the infection focus is observed. It seems that the failure of neutrophil migration is dependent on toll-like receptor 4 (TLR4) and mediated by cytokines and chemokines, which induce the production of nitric oxide that inhibits neutrophil adhesion to venular endothelium and also the neutrophil chemotactic ability.
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Cite this article as:
Alves-Filho C. J., Tavares-Murta M. B., Barja-Fidalgo C., Benjamim F. C., Basile-Filho A., Arraes M. S. and Cunha Q. F., Neutrophil Function in Severe Sepsis, Endocrine, Metabolic & Immune Disorders - Drug Targets 2006; 6 (2) . https://dx.doi.org/10.2174/187153006777442404
DOI https://dx.doi.org/10.2174/187153006777442404 |
Print ISSN 1871-5303 |
Publisher Name Bentham Science Publisher |
Online ISSN 2212-3873 |
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