SOLUBLE CYTOKINE RECEPTORS AND RECEPTOR ANTAGONISTS ARE SEQUENTIALLY RELEASED AFTER TRAUMA
SOLUBLE CYTOKINE RECEPTORS AND RECEPTOR ANTAGONISTS ARE SEQUENTIALLY RELEASED AFTER TRAUMA
复制标题
DOI：
10.1097/00005373-199507000-00015
复制
发表时间：
1995-07-01
影响因子：
--
通讯作者：
TOMINAGA, GT
中科院分区：
文献类型：
--
作者：
CINAT, M;WAXMAN, K;TOMINAGA, GT
细胞因子受体和受体拮抗剂（RA）已被确定在创伤患者。我们假设，创伤性损伤后，可溶性细胞因子受体和RA的顺序释放可能存在，反映了主要细胞因子本身的释放。本研究纳入了22例患者：14例男性和8例女性。平均年龄为30.1 ± 12.5（范围：19 - 71），平均损伤严重度评分为28.7 ± 12.6（范围：4 - 57）。存活15例，死亡7例。在到达急诊科时收集样本，并连续间隔长达7天。采用抗肿瘤坏死因子（TNF）、可溶性TNF受体（sTNF-R）55 kd和75 kd、白细胞介素（IL）-1和IL-1 RA、IL-2和IL-2 r单克隆抗体酶联免疫吸附试验试剂盒。22例健康人血清作为正常对照。损伤后任何患者血清中均未检测到TNF、IL-1或IL-2。可溶性细胞因子受体和RA的对照水平如下：sTNF-R 55 kd，607 +/- 89 pg/mL; sTNF-R 75 kd，2，141 +/- 169 pg/mL; IL-1 RA，291 +/- 35 pg/mL;和IL-2 r，426 +/- 53 U/mL。在创伤患者中，55 kd和75 kd sTNF-R在到达急诊室时均显著升高，数值分别为2，441 +/- 506 pg/mL（p < 0.001）和4，736 +/- 537 pg/mL（p < 0.001）。尽管IL-1 IWs在到达急诊科时也显著升高，但血清水平继续升高，在损伤后4至6小时达到峰值，数值为58，257 +/-22，841 pg/mL（p < 0.005）。相比之下，IL-2 r水平在7至12小时达到峰值，为624 +/- 71 U/mL 05）;在第1，757 +/- 51 U/mL（p < 0.001）;在第4天，1，063 +/- 217 U/mL（p < 0.001）;和在第7天，2，337 +/- 815 U/mL（p < 0.001）。这些数据表明，尽管缺乏可检测水平的主要细胞因子本身，但细胞因子受体和RA仍顺序释放。可能存在一种以前未被认识到的生理机制来调节损伤后细胞因子受体和RA的释放。
Cytokine receptors and receptor antagonists (RAs) have been identified in trauma patients. We hypothesized that after traumatic injury, a sequential release of soluble cytokine receptors and RAs may exist that mirrors the release of the primary cytokines themselves. Twenty-two patients were included in the study: 14 males and 8 females. The mean age was 30.1 +/- 12.5 (range, 19 to 71), and the mean Injury Severity Score was 28.7 +/- 12.6 (range,4 to 57). There were 15 survivors and 7 nonsurvivors. Samples were collected on arrival to the emergency department and at serial intervals for up to 7 days. Monoclonal antibody enzyme-linked immunosorbent assay kits to tumor necrosis factor (TNF), soluble TNF-receptor (sTNF-R) 55 kd and 75 kd, interleukin (IL)-1 and IL-1 RA, and IL-2 and IL-2r were used. Sera from 22 healthy individuals were used as normal controls. No TNF, IL-1, or IL-2 could be detected in any patient sera after injury. Control levels for the soluble cytokine receptors and RAs were as follows: sTNF-R 55 kd, 607 +/- 89 pg/mL; sTNF-R 75 kd, 2,141 +/- 169 pg/mL; IL-1 RA, 291 +/- 35 pg/mL; and IL-2r, 426 +/- 53 U/mL. In trauma patients, both 55 kd and 75 kd sTNF-R were significantly elevated on arrival to the emergency department, with values of 2,441 +/- 506 pg/mL (p < 0.001) and 4,736 +/- 537 pg/mL (p < 0.001), respectively. Although IL-1 IWs were also significantly elevated on arrival to the emergency department, serum levels continued to rise, peaking 4 to 6 hours after injury, with values of 58,257 +/- 22,841 pg/mL (p < 0.005). In contrast, IL-2r levels peaked later, with values at 7 to 12 hours, 624 +/- 71 U/mL (p < 0.05); at day 1,757 +/- 51 U/mL (p < 0.001); at day 4,1,063 +/- 217 U/mL (p < 0.001); and at day 7, 2,337 +/- 815 U/mL (p < 0.001). These data suggest a sequential release of cytokine receptors and RAs, despite the absence of detectable levels of the primary cytokines themselves. A previously unrecognized physiologic mechanism may exist that regulates cytokine receptor and RA release after injury.