Cellular Immunodepression Preceding Infectious Complications after Acute Ischemic Stroke in Humans

作者：Karl Georg Hæusler, Wolf Ulrich Schmidt, Fabian Föhring, Christian Meisel, Thomas M. Helms, G. J. Jungehülsing, Christian Hans Nolte, Katrin Schmolke, Brigitte Wegner, Andreas Meisel, Ulrich Dirnagl, Arno Villringer, Hans‐Dieter Volk · 发表于：Cerebrovascular Diseases · 年份：2007 · DOI：10.1159/000111499 · 被引用次数：234 · 研究领域：Neuroinflammation and Neurodegeneration Mechanisms、Acute Ischemic Stroke Management、Immune Response and Inflammation

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.