Early neutrophil sequestration after injury: a pathogenic mechanism for multiple organ failure.
Early neutrophil sequestration after injury: a pathogenic mechanism for multiple organ failure.
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DOI：
10.1097/00005373-199509000-00003
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发表时间：
1995-09
期刊：
影响因子：
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通讯作者：
Abraham J. Botha;F. Moore;Ernest E. Moore;A. Sauaia;A. Banerjee;V. Peterson
中科院分区：
文献类型：
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作者：
Abraham J. Botha;F. Moore;Ernest E. Moore;A. Sauaia;A. Banerjee;V. Peterson
中性粒细胞(PMN)在多器官衰竭(MOF)前的炎症反应中起着关键作用。在多器官功能衰竭的大鼠模型中，中性粒细胞准备增加超氧阴离子(O2-)释放和CD11b表达，隔离在终末器官，并产生器官衰竭。因此，我们假设在创伤后24小时内从有MOF风险的创伤患者采集的循环PMN将(1)显示启动的O2-释放，(2)上调CD11b的表达，以及(3)显示组织中隔离的证据。检测33例躯干创伤患者伤后3、6、12、24小时的细胞外PMN O2-释放和CD11b受体表达，其中8例(24%)发生多器官功能衰竭。健康成人作为对照。损伤后的中性粒细胞在损伤后3、6、12和24小时准备增强体外O2-释放，这表明之前在体内进行了准备。CD11b在伤后6、12、24小时表达增强。外周血中中性粒细胞数量在伤后3小时急剧增加，在6小时和12小时急剧下降，提示器官隔离已结束。伤后12小时，多器官功能衰竭患者外周血中中性粒细胞的下降明显大于非多器官功能衰竭患者(p<；0.05)。这些数据表明，中性粒细胞在损伤后迅速动员到循环中，然后为增强O2-释放和CD11b表达做好准备。PMN启动似乎是躯干严重创伤患者PMN隔离的必要前奏。PMN功能上调，伴随着随后的终末器官隔离，可能是创伤后MOF发病机制中的一个重要早期事件。
Polymorphonuclear neutrophils (PMNs) play a pivotal role in the inflammation that precedes multiple organ failure (MOF). In a rat model of MOF, PMNs become primed for enhanced superoxide anion (O2-) release and CD11b expression, sequester in end organs, and produce organ failure. Therefore, we hypothesized that circulating PMNs harvested in the first 24 hours after injury from trauma patients at risk for MOF would (1) exhibit a primed O2- release, (2) upregulate CD11b expression, and (3) show evidence of sequestration in tissues. Extracellular PMN O2- release and CD11b receptor expression were measured at 3, 6, 12, and 24 hours after injury in 33 torso trauma patients with Injury Severity Scores > 15; eight patients (24%) developed MOF. Healthy adults served as controls. PMNs after injury were primed for enhanced in vitro O2- release at 3, 6, 12, and 24 hours after injury, indicating prior in vivo priming. CD11b expression was also increased at 6, 12, and 24 hours after injury. Circulating PMN numbers increased sharply at 3 hours after injury, before decreasing dramatically at 6 and 12 hours, suggesting end organ sequestration. At 12 hours after injury, declines in circulating PMNs were significantly greater in MOF than in non-MOF patients (p < 0.05). These data indicate that PMNs are quickly mobilized into the circulation after injury and then primed for enhanced O2- release and CD11b expression. PMN priming appears to be a necessary preamble to PMN sequestration in patients with major torso trauma. Upregulation of PMN function, accompanied by subsequent end organ sequestration, may represent an important early event in the pathogenesis of MOF after injury.