Cellular immunodepression preceding infectious complications after acute ischemic stroke in humans

Cellular immunodepression preceding infectious complications after acute ischemic stroke in humans
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DOI:
10.1159/000111499
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发表时间:
2008-01-01
影响因子:
2.9
通讯作者:
Volk, Hans-Dieter
Volk, Hans-Dieter
中科院分区:
医学3区
文献类型:
--
作者:
Haeusler, Karl Georg;Schmidt, Wolf U. H.;Volk, Hans-Dieter

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背景:我们最近的研究表明,缺血性中风在小鼠中引起应激介质诱导的长期免疫抑制状态。方法:采用头部磁共振成像和标准化免疫测定,我们前瞻性地研究脑卒中后免疫抑制是否也见于人类。结果:与健康志愿者(n = 30)相比,急性卒中患者(SP; n = 40)淋巴细胞计数迅速下降,单核细胞和辅助性T型1细胞功能失活。免疫抑制在严重临床缺陷或大面积梗死患者中更为明显。入院时,单核细胞肿瘤坏死因子α体外释放和美国国立卫生研究院卒中量表评分是院内感染的最佳预测指标,优先影响老年SP。结论:我们的数据为人类缺血性卒中后细胞介导的免疫反应的立即抑制提供了证据。版权所有(c) 2007 S. Karger AG,巴塞尔。
Background: We have recently shown that ischemic stroke causes a stress-mediator-induced long-lasting immunodepressive state in mice. Methods: Using head magnetic resonance imaging and standardized immunoassays, we prospectively investigated whether poststroke immunodepression is also seen in humans. Results: Compared to healthy volunteers (n = 30), a rapid depression of lymphocyte counts and a functional deactivation of monocytes and T helper type 1 cells was observed in acute stroke patients (SP; n = 40). Immunodepression was more pronounced in patients with severe clinical deficit or large infarction. On admission the combination of monocytic tumor necrosis factor alpha release ex vivo and the National Institute of Health Stroke Scale score were the best predictors for nosocomial infection, preferentially affecting older SP. Conclusion: Our data provide evidence for an immediate suppression of cell-mediated immune responses after ischemic stroke in humans. Copyright (c) 2007 S. Karger AG, Basel.