Inappropriate activation, deactivation, and probable autooxidative damage as a mechanism of neutrophil locomotory defect in trauma.
Inappropriate activation, deactivation, and probable autooxidative damage as a mechanism of neutrophil locomotory defect in trauma.
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不适当的激活、失活和可能的自氧化损伤是创伤中中性粒细胞运动缺陷的机制。
DOI：
10.1093/infdis/154.3.471
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Pock,RM
中科院分区：
文献类型：
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作者：
Maderazo,EG;Woronick,CL;Albano,SD;Breaux,SP;Pock,RM
我们研究了46例严重钝伤患者，以探讨其获得性中性粒细胞（PMN）运动功能障碍的可能机制。患者血浆C3 adeSAg浓度高于对照组（分别为310 ± 190 ng/ml vs. 90 ± 28 ng/ml;P= 3 × 10-5）。患者的静息和吞噬PMN均产生较高量的H202（分别为0.31 × 0.29和5.2 × 3.4 nmol/106 PMN/hr）。这些水平与用趋化因子预活化的正常PMNs产生H20 2的水平相似（正常PMNs为0.85 ± 0.03 nmol/10 6）h，预活化PMNs为8.2 ± 1.6 nmol/10 6）h。患者PMN中氧化型谷胱甘肽的浓度与对照组PMN相比并不显著更高（分别为0.053 ± 0.057 vs. 0.037 ± 0.046 nmol/106 PMN;P= 0.5）。与对照组相比，创伤患者的PMN被伴刀豆球蛋白A覆盖的百分比更高（分别为66% ± 11%和37% ± 14%;P= 4 × 10-5），这一结果表明微管功能障碍。这些结果表明，在创伤，血管内补体激活的结果在不适当的趋化刺激和随后的失活和循环中性粒细胞的自氧化损伤。
We studied 46 patients who suffered from serious blunt trauma to examine the possible mechanism of their acquired neutrophil (PMN) locomotory dysfunction. Concentrations of plasma C3adeSArgwere higher in patients than in controls (310 ± 190 ng/ml vs. 90 ± 28 ng/ml, respectively;P= 3 × 10-5) . Both resting and phagocytosing PMNs from the patients produced higher quantities of H202(0.31 × 0.29 and 5.2 × 3.4 nmol/106PMNs per hr, respectively). These levels resemble the H 20 2 production of normal PMNs preactivated with chemotactic factor (0.85 ± 0.03 for normal and 8.2 ± 1.6 nmol/106) PMNs per hr for preactivated PMNs). Concentrations of oxidized glutathione were not significantly higher in PMNs from patients compared with PMNs from controls (0.053 ± 0.057 vs. 0.037 ± 0.046 nmol/106PMNs, respectively;P= .5). A higher percentage of PMNs from trauma patients than from controls were capped with concanavalin A (66% ± 11% vs. 37% ± 14%, respectively;P= 4 × 10-5), a result indicating microtubular dysfunction. These findings suggest that in trauma, activation of intravascular complement results in inappropriate chemotactic stimulation and subsequent deactivation and autoxidative damage of circulating PMNs.