IL-10 levels in cerebrospinal fluid and serum of patients with severe traumatic brain injury:: relationship to IL-6, TNF-α, TGF-β1 and blood-brain barrier function
IL-10 levels in cerebrospinal fluid and serum of patients with severe traumatic brain injury:: relationship to IL-6, TNF-α, TGF-β1 and blood-brain barrier function
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DOI：
10.1016/s0165-5728(99)00148-4
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发表时间：
1999-11-15
影响因子：
3.3
通讯作者：
Kossmann, T
中科院分区：
文献类型：
--
作者：
Csuka, E;Morganti-Kossmann, MC;Kossmann, T
控制脑损伤后炎症反应的程度可能是有益的，因为创伤后颅内炎症与不良后果有关。为了阐明抗炎介质的潜在作用，我们监测了28例严重创伤性脑损伤（TBI）患者脑脊液（CSF）和血清中白细胞介素-10 （IL-10）的产生，并与对照组进行了比较。在长达22天的时间内，分析了两种液体中IL-10的模式与IL-6、肿瘤坏死因子- α (tnf - α)和转化生长因子- β 1 （tgf - β 1）的模式。同时，使用CSF-/血清白蛋白商（Q(A)）监测血脑屏障（BBB）的功能/功能障碍，并与鞘内细胞因子水平进行比较。与对照组相比，28例TBI患者中有26例（范围：1.3-41.7 pg/ml）脑脊液中IL-10平均浓度升高（临界值：1.06 pg/ml），而只有7例患者血清中IL-10平均浓度升高（范围：5.4-23 pg/ml；临界值：5.14 pg/ml）。两种液体中IL-10的时间过程相似，在第一天出现峰值，第二周出现较低的上升。假设鞘内IL-10合成，因为大多数患者CSF-IL-10水平超过血清IL-10水平，IL-10指数（CSF/血清IL-10/Q(A)）在23例患者中升高，并且CSF-IL-10的升高显示与严重的血脑屏障功能障碍无关。脑脊液和血清IL-10值均与血脑屏障功能障碍无关。随着时间的推移，IL-10、IL-6和tgf - β 1在脑脊液中表现出相似的模式，而tnf - α的升高与IL-10水平的下降相对应。我们的研究结果表明，IL-10主要是在严重脑外伤后鞘内诱导的，它可能下调创伤性脑损伤后的炎症事件。(C) 1999 Elsevier Science B.V.版权所有
Controlling the extent of inflammatory responses following brain injury may be beneficial since posttraumatic intracranial inflammation has been associated with adverse outcome. In order to elucidate the potential role of anti-inflammatory mediators, the production of interleukin-10 (IL-10) was monitored in paired cerebrospinal fluid (CSF) and serum of 28 patients with severe traumatic brain injury (TBI) and compared to control samples. The pattern of IL-10 was analyzed with respect to the patterns of IL-6, tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) in both fluids during a time period of up to 22 days. In parallel, the function/dysfunction of the blood-brain barrier (BBB) was monitored using the CSF-/serum-albumin quotient (Q(A)) and compared to intrathecal cytokine levels. Mean IL-10 concentration in CSF was elevated in 26 out of 28 TBI patients (range: 1.3-41.7 pg/ml) compared to controls (cut-off: 1.06 pg/ml), whereas only seven patients had elevated mean IL-10 concentration in serum (range: 5.4-23 pg/ml; cut-off: 5.14 pg/ml). The time course of IL-10 was similar in both fluids, showing a peak during the first days and a second, lower rise in the second week. Intrathecal IL-10 synthesis is hypothesized since CSF-IL-10 levels exceeded serum-IL-10 levels in most of the patients, IL-10-index (CSF/serum-IL-10/Q(A)) was elevated in 23 individuals, and elevation of CSF-IL-10 showed to be independent from severe BBB dysfunction. Neither CSF nor serum IL-10 values correlated with the dysfunction of the BBB. IL-10, IL-6 and TGF-beta 1 showed similar patterns in CSF over time, whereas rises of TNF-alpha corresponded to declines of IL-10 levels. Our results suggest that IL-10 is predominantly induced intrathecally after severe TBI where it may downregulate inflammatory events following traumatic brain damage. (C) 1999 Elsevier Science B.V. All rights reserved.