Priming, second-hit priming, and apoptosis in leukocytes from trauma patients
Priming, second-hit priming, and apoptosis in leukocytes from trauma patients
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DOI：
10.1097/00005373-199905000-00004
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发表时间：
1999-05-01
影响因子：
--
通讯作者：
Sugimoto, H
中科院分区：
文献类型：
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作者：
Ogura, H;Tanaka, H;Sugimoto, H
背景：多形核白细胞（polymorphisms leukocytes，PMNL）在宿主防御和损伤后的全身炎症反应中起重要作用.本研究的目的是研究严重创伤患者PMNL启动和细胞凋亡的系列变化，并评估第二次打击对启动PMNL功能和全身血管内皮损伤的影响。方法：24例严重创伤患者（平均损伤严重程度评分，31.1 +/- 9.7）。在7名患者中，感染被视为创伤后的第二次打击。用流式细胞仪检测PMNL的氧化活性、吞噬功能和凋亡，分别以无刺激和有甲酰甲硫氨酰-亮氨酰-苯丙氨酸（FMLP）刺激时的氧化活性作为启动指标和FMLP反应。结果：PMNL激发指数在伤后2 ~ 13天升高，尤以伤后2 ~ 5天升高最明显，伤后2 ~ 13天升高最明显，伤后2 ~ 5天升高最明显。FMLP反应在伤后2 ~ 21天增强。PMNL细胞凋亡在伤后3周内一直受到抑制。创伤后第二次感染在诊断感染后24小时内增强了启动指数和FMLP反应，并增加了血清IL-6浓度。然而，血清血栓调节蛋白水平不受第二次打击。结论：严重创伤刺激PMNL急性期启动并抑制细胞凋亡，创伤后感染诱导PMNL二次启动，但血栓调节蛋白水平无变化，提示启动本身可能不引起系统性血管内皮损伤。
Background: Polymorphonuclear leukocytes (PMNL) play important roles in both host defenses and systemic inflammatory responses after insults. The objectives of this study are to examine the serial changes in PMNL priming and apoptosis in severely injured patients and to evaluate the impact of second hits on primed PMNL function and systemic vascular endothelial damage.Methods: Twenty-four severely injured patients (mean Injury Severity Score, 31.1 +/- 9.7) were included. Infections were seen as second hits after trauma in seven patients. Oxidative activity, phagocytosis, and apoptosis of PMNL from serial blood samples were measured by flow cytometry, Oxidative activity with no stimulus and with formylmethionyl-leucyl-phenylalanine (FMLP) were analyzed as the priming index and FMLP response, respectively. Interleukin (IL)-6, IL-10, PMNL elastase, and thrombomodulin concentrations in blood were also measured before and after the second hit.Results: The PMNL priming index was elevated from days 2 to 13, especially days 2 to 5 after injury. FMLP response was enhanced from days 2 to 21 after injury. Apoptosis of PMNL was inhibited for as long as 3 weeks after injury. Infections as second hits after trauma enhanced both the priming index and the FMLP response within 24 hours after diagnosis of infection and increased serum IL-6 concentrations. However, serum thrombomodulin levels were not affected by second hits. All patients with second hits survived.Conclusion: Severe trauma stimulated acute-phase priming in PMNL and inhibited apoptosis, Infections after trauma induced second-hit priming in PMNL, but the unchanged serum levels of thrombomodulin suggest that priming per se may not cause systemic vascular endothelial damage.