Jaeschke H, Smith C W
Pharmacia & Upjohn, Inc., Kalamazoo, Michigan 49007, USA.
J Leukoc Biol. 1997 Jun;61(6):647-53. doi: 10.1002/jlb.61.6.647.
Neutrophils are involved in organ damage induced by an excessive acute inflammatory response after ischemia-reperfusion, trauma, and sepsis. In addition to causing vascular injury, neutrophils can transmigrate and attack parenchymal cells. This review summarizes recent advances in our understanding of neutrophil-induced parenchymal cell injury using the liver as an example. Reviewed are the mechanisms of neutrophil sequestration in the hepatic vasculature, transendothelial migration, adherence to hepatic parenchymal cells, and mechanisms of cytotoxicity. Discussed are the involvement of various adhesion molecules in these processes, the role of cytokines and chemokines in the pathophysiology, as well as the effects of proteases and reactive oxygen species released by neutrophils. The emerging understanding of the basic mechanisms of neutrophil-induced organ damage is critical for the development of therapeutic strategies to attenuate excessive acute inflammatory responses without compromising essential host defense mechanisms.
中性粒细胞参与缺血再灌注、创伤和脓毒症后过度急性炎症反应所导致的器官损伤。除了引起血管损伤外，中性粒细胞还可迁移并攻击实质细胞。本综述以肝脏为例，总结了我们对中性粒细胞诱导实质细胞损伤的最新认识进展。回顾了中性粒细胞在肝血管系统中滞留、跨内皮迁移、黏附于肝实质细胞的机制以及细胞毒性机制。讨论了各种黏附分子在这些过程中的作用、细胞因子和趋化因子在病理生理学中的作用，以及中性粒细胞释放的蛋白酶和活性氧的影响。对中性粒细胞诱导器官损伤基本机制的新认识对于制定治疗策略以减轻过度急性炎症反应而不损害基本宿主防御机制至关重要。
