HMGB1 is markedly elevated within 6 hours of mechanical trauma in humans.
HMGB1 is markedly elevated within 6 hours of mechanical trauma in humans.
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DOI：
10.1097/shk.0b013e3181997173
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发表时间：
2009-07
期刊：
影响因子：
--
通讯作者：
Abraham E
中科院分区：
文献类型：
--
作者：
Peltz ED;Moore EE;Eckels PC;Damle SS;Tsuruta Y;Johnson JL;Sauaia A;Silliman CC;Banerjee A;Abraham E
高迁移率族蛋白 1 (HMGB1) 是与脓毒症相关的全身炎症的晚期介质。最近，HMGB1 在动物体内被证明是出血引起的器官功能障碍的介质。然而，人类创伤后血浆 HMGB1 升高的时间过程仍有待阐明。因此，我们假设人类的机械创伤会导致血浆 HMGB1 早期显着升高。确定纳入具有多器官衰竭风险（ISS ≥15）的创伤患者（n = 23），并通过酶联免疫吸附测定法对损伤后血浆样本进行 HMGB1 测定。将损伤后 HMGB1 水平与患者结局标志物（年龄、损伤严重程度评分、每前 24 小时输注的红细胞 (RBC) 单位以及碱基缺乏）进行比较。为了研究损伤后输血是否导致循环 HMGB1 升高，测定了白细胞减少和非白细胞减少的浓缩红细胞中的水平。受伤后 1 小时内，血浆 HMGB1 比健康对照升高 30 倍以上（中位数为 57.76 与 1.77 ng/mL；P < 0.003），在损伤后 2 至 6 小时达到峰值（中位数为 526.18 ng/mL；与对照相比，P < 0.01），并在 136 小时内保持高于对照的升高状态。损伤后 HMGB1 水平与患者预后标志物之间没有明显的关系。高迁移率组盒 1 的水平随着红细胞储存时间的延长而增加，尽管其浓度并未考虑到受伤后的血浆水平。白细胞减少了浓缩红细胞中 HMGB1 水平约 55% (P < 0.01)。人类创伤后 1 小时内，血浆 HMGB1 显着升高，且在受伤后 2 至 6 小时内显着升高。这些结果表明，与败血症相反，HMGB1 释放是人类创伤后的早期事件。因此，HMGB1可能是创伤早期炎症反应不可或缺的一部分，并且是未来治疗的潜在靶点。
High-mobility group box 1 (HMGB1) is a late mediator of the systemic inflammation associated with sepsis. Recently, HMGB1 has been shown in animals to be a mediator of hemorrhage-induced organ dysfunction. However, the time course of plasma HMGB1 elevations after trauma in humans remains to be elucidated. Consequently, we hypothesized that mechanical trauma in humans would result in early significant elevations of plasma HMGB1. Trauma patients at risk for multiple organ failure (ISS ≥15) were identified for inclusion (n = 23), and postinjury plasma samples were assayed for HMGB1 by enzyme-linked immunosorbent assay. Comparison of postinjury HMGB1 levels with markers for patient outcome (age, injury severity score, units of red blood cell (RBC) transfused per first 24 h, and base deficit) was performed. To investigate whether postinjury transfusion contributes to elevations of circulating HMGB1, levels were determined in both leuko-reduced and non–leuko-reduced packed RBCs. Plasma HMGB1 was elevated more than 30-fold above healthy controls within 1 h of injury (median, 57.76 vs. 1.77 ng/mL; P < 0.003), peaked from 2 to 6 h postinjury (median, 526.18 ng/mL; P < 0.01 vs. control), and remained elevated above control through 136 h. No clear relationship was evident between postinjury HMGB1 levels and markers for patient outcome. High-mobility group box 1 levels increase with duration of RBC storage, although concentrations did not account for postinjury plasma levels. Leuko-reduced attenuated HMGB1 levels in packed RBCs by approximately 55% (P < 0.01). Plasma HMGB1 is significantly increased within 1 h of trauma in humans with marked elevations occurring from 2 to 6 h postinjury. These results suggest that, in contrast to sepsis, HMGB1 release is an early event after traumatic injury in humans. Thus, HMGB1 may be integral to the early inflammatory response to trauma and is a potential target for future therapeutics.
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影响因子：
4.4
作者：
Sha, Yonggang;Zmijewski, Jaroslaw;Abraham, Edward
通讯作者：
Abraham, Edward
DOI：
10.1097/00005373-199502000-00006
发表时间：
1995-02-01
影响因子：
--
作者：
SAUAIA, A;MOORE, FA;PONS, PT
通讯作者：
PONS, PT
DOI：
10.1152/ajplung.00359.2004
发表时间：
2005-05-01
影响因子：
4.9
作者：
Kim, JY;Park, JS;Abraham, E
通讯作者：
Abraham, E
影响因子：
38.9
作者：
Gibot, Sebastien;Massin, Frederic;Bollaert, Pierre-Edouard
通讯作者：
Bollaert, Pierre-Edouard
影响因子：
5.5
作者：
Park, JS;Arcaroli, J;Abraham, E
通讯作者：
Abraham, E