Yearbook of Intensive Care and Emergency Medicine

Volume 1996 of the series Yearbook of Intensive Care and Emergency Medicine pp 83-95

Neutrophil-induced Oxidative Stress

  • M. Lamy
  • , M. Mathy-Hartert
  • , G. Deby-Dupont

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The respiratory burst of neutrophils, as well as their degranulation, constitutes a defensive response to tissue damage, whether induced by mechanical, chemical, or infectious stimuli [1]. This response, which is normally tightly regulated, leads to leukocyte migration into the area of damage [2]. Macrophages, polymorphonuclear neutrophils (PMN), and lymphocytes are recruited and stimulated, with concomitant production of soluble mediators (cytokines, prostanoids, leukotrienes, acute phase reactant proteins, etc.). This response is beneficial for the organism, because it leads to the phagocytosis of microorganisms and foreign material, lysis within phagolysosomes, and production of antibodies by lymphocytes. The vascular endothelium is also involved in this beneficial response, because local inflammation is associated with vasodilation and diapedesis of neutrophils across the vascular wall into the inflammatory focus. Specific receptors, both on the neutrophils and the endothelial cells play an important role in any inflammatory process [3–6].