Clinical outcome following acute ischaemic stroke relates to both activation and autoregulatory inhibition of cytokine production.
Clinical outcome following acute ischaemic stroke relates to both activation and autoregulatory inhibition of cytokine production.
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DOI：
10.1186/1471-2377-7-5
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发表时间：
2007-02-28
期刊：
影响因子：
2.6
通讯作者：
Hopkins SJ
中科院分区：
文献类型：
--
作者：
Emsley HC;Smith CJ;Gavin CM;Georgiou RF;Vail A;Barberan EM;Illingworth K;Scarth S;Wickramasinghe V;Hoadley ME;Rothwell NJ;Tyrrell PJ;Hopkins SJ
作为局部和全身炎症反应的关键介质，细胞因子在缺血性脑卒中后的大脑中产生。有些已经在中风患者的血液循环中检测到，但它们的作用和来源尚不清楚。主要关注白细胞介素(IL)-1相关机制，我们连续测量了36例急性缺血性卒中（AIS）后12小时内招募的患者血浆炎症标志物和全血细胞因子的产生，并随访至1年。入院时血浆IL-1受体拮抗剂（IL-1ra）浓度升高，相对于年龄、性别和动脉粥样硬化匹配的对照组。IL-1β、可溶性IL-1受体II型、肿瘤坏死因子(TNF)-α、TNF- rii、IL-10和瘦素浓度与对照组无显著差异，但第一周可溶性TNF-受体I型（sTNF-RI）峰值与5-7天的计算机断层扫描梗死体积、3个月和12个月的mRS和BI密切相关。与对照组相比，5-7天的患者和有明显动脉粥样硬化的患者的新蝶呤水平升高。自发的IL-1β、TNF-α和IL-6基因和蛋白在血细胞中的表达很少，并且在第一周内，脂多糖（LPS）对这些细胞因子的诱导明显低于对照组。最低脂多糖诱导的细胞因子产生与mRS和BI以及血浆皮质醇密切相关。缺乏自发的全血基因激活或细胞因子产生表明外周血细胞不是AIS后血浆中细胞因子的来源。AIS发病后12小时内血浆IL-1ra升高、sTNF-RI与卒中严重程度的关系以及细胞因子诱导抑制提示AIS后内源性免疫抑制机制的早期激活。
As critical mediators of local and systemic inflammatory responses, cytokines are produced in the brain following ischaemic stroke. Some have been detected in the circulation of stroke patients, but their role and source is unclear. Focusing primarily on interleukin(IL)-1-related mechanisms, we serially measured plasma inflammatory markers, and the production of cytokines by whole blood, from 36 patients recruited within 12 h and followed up to 1 year after acute ischaemic stroke (AIS). Admission plasma IL-1 receptor antagonist (IL-1ra) concentration was elevated, relative to age-, sex-, and atherosclerosis-matched controls. IL-1β, soluble IL-1 receptor type II, tumour necrosis factor (TNF)-α, TNF-RII, IL-10 and leptin concentrations did not significantly differ from controls, but peak soluble TNF receptor type I (sTNF-RI) in the first week correlated strongly with computed tomography infarct volume at 5–7 days, mRS and BI at 3 and 12 months. Neopterin was raised in patients at 5–7 d, relative to controls, and in subjects with significant atherosclerosis. Spontaneous IL-1β, TNF-α and IL-6 gene and protein expression by blood cells was minimal, and induction of these cytokines by lipopolysaccharide (LPS) was significantly lower in patients than in controls during the first week. Minimum LPS-induced cytokine production correlated strongly with mRS and BI, and also with plasma cortisol. Absence of spontaneous whole blood gene activation or cytokine production suggests that peripheral blood cells are not the source of cytokines measured in plasma after AIS. Increased plasma IL-1ra within 12 h of AIS onset, the relationship between sTNF-RI and stroke severity, and suppressed cytokine induction suggests early activation of endogenous immunosuppressive mechanisms after AIS.
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DOI：
10.1073/pnas.96.12.7047
发表时间：
1999-06-08
影响因子：
11.1
作者：
Luheshi, GN;Gardner, JD;Rothwell, NJ
通讯作者：
Rothwell, NJ
影响因子：
11.2
作者：
Castillo, J;Moro, MA;Dávalos, A
通讯作者：
Dávalos, A
影响因子：
3.1
作者：
Bergmann, M;Gornikiewicz, A;Függer, R
通讯作者：
Függer, R
影响因子：
8.3
作者：
Langhorne, P;Stott, DJ;Murray, G
通讯作者：
Murray, G
DOI：
10.1097/00004647-199909000-00008
发表时间：
1999-09-01
影响因子：
6.3
作者：
Ferrarese, C;Mascarucci, P;De Simoni, MG
通讯作者：
De Simoni, MG