Deficient transforming growth factor β and interleukin-10 responses contribute to the septic death of burned patients
Deficient transforming growth factor β and interleukin-10 responses contribute to the septic death of burned patients
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DOI：
10.1016/s0305-4179(02)00113-4
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发表时间：
2002-11-01
期刊：
影响因子：
2.7
通讯作者：
Fang, RH
中科院分区：
文献类型：
--
作者：
Yeh, FL;Shen, HD;Fang, RH
为了了解促炎和抗炎细胞因子在烧伤损伤和烧伤后脓毒症中的作用，我们测定了15例烧伤患者血清转化生长因子β -1 （tgf -1）水平的系列变化，并与IL-6和IL-10水平进行了比较。15例患者中8例痊愈无脓毒症。另外7人因脓毒症死亡。我们的研究结果显示，在烧伤后1天内检测到初始血清tgf - β -1反应峰值。血清IL-6和IL-10的峰值也在这些患者烧伤后4天内检测。血清IL-6、IL-10和tgf - β -1的峰值水平在总体表面积（TBSA）大于或小于50%的患者以及烧伤存活或死亡患者之间无显著差异。之后，幸存者体内循环IL-6和IL-10的水平仍然很低。然而，在所有被分析的烧伤患者中，血清tgf - β -1水平出现了第二个高峰反应。8名幸存者和7名非幸存者烧伤后血清tgf - β -1水平的第二个峰值分别为28,542至76,554 pg/ml（平均值为51,256至14,264 pg/ml）和8616至40,851 pg/ml（平均值为24079至10,399 pg/ml）。存活组与非存活组间第二峰tgf - β -1反应平均值差异有统计学意义（P < 0.01）。脓毒症患者的循环IL-6水平在烧伤后1-2周呈上升趋势，并在患者到期前达到较高水平。在最初的高峰反应后，7名非幸存者中的1名血清IL-10水平仍然很低，而其他6名非幸存者的血清IL-10水平则有所上升。然而，循环IL-10水平的显著增加仅在这些非幸存者死亡前观察到。总之，烧伤后检测到血清IL-6、IL-10和tgf - β -1水平的初始升高。死亡前血清IL-6水平的显著升高提示其在烧伤患者脓毒症病理生理中的作用。此外，在非幸存者中继发性tgf - β -1反应低和循环IL-10缺乏和/或延迟增加可能都有助于烧伤患者脓毒性死亡的病理生理学。(C) 2002 Elsevier Science Ltd和ISBI。版权所有。
In order to understand the roles of pro-inflammatory and anti-inflammatory cytokines in burn injury and sepsis post-burn, serial changes in serum levels of transforming growth factor beta-1 (TGF-beta-1) were determined and compared to those of IL-6 and IL-10 in 15 burned patients. Among these 15 patients, 8 recovered without sepsis. The other seven, who were septic, expired. Our results showed that an initial peak serum TGF-beta-1 response was detected within 1 day post-burn. Peak serum IL-6 and IL-10 responses were also detected within 4 days after the burn injury of these patients. Significant differences in peak serum IL-6, IL-10 and TGF-beta-1 levels were not found between patients with total body surface area (TBSA) of greater or less than 50% and between patients who survived or expired from burn injury. Afterwards, levels of circulating IL-6 and IL-10 remained low in the survivors. However, a second peak response in serum TGF-beta-1 levels was observed in all burned patients analyzed. The second peak serum TGF-beta-1 levels post-burn of the eight survivors and the seven non-survivors were from 28,542 to 76,554 pg/ml (a mean value of 51,256 14,264 pg/ml) and from 8616 to 40,851 pg/ml (a mean value of 24,079 10,399 pg/ml), respectively. A significant difference (P < 0.01) in mean values of the second peak TGF-beta-1 responses between groups of survivors and non-survivors was detected. Levels of circulating IL-6 in the septic non-surviving patients showed a tendency to increase 1-2 weeks post-burn and reached high levels before the expiration of these patients. After an initial peak response, the serum IL-10 level remained low in one of the seven non-survivors, while it increased in the other six non-survivors. However, marked increases in circulating IL-10 levels were observed only just before the death of these non-survivors. In conclusion, an initial increase in serum levels of IL-6, IL-10 and TGF-beta-1 was detected post-burn. A marked increase in serum levels of IL-6 before death suggests its role in the pathophysiology of sepsis in burned patients. In addition, a low secondary TGF-beta-1 response and a lack and/or delay in the increase of circulating IL-10 in the non-survivors may all contribute to the pathophysiology of septic death in burned patients. (C) 2002 Elsevier Science Ltd and ISBI. All rights reserved.