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Cellular immunodepression preceding infectious complications after acute ischemic stroke in humans

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Citation

Haeusler, K. G., Schmidt, W. U., Foehring, F., Meisel, C., Helms, T., Jungehulsing, G. J., et al. (2008). Cellular immunodepression preceding infectious complications after acute ischemic stroke in humans. Cerebrovascular Diseases, 25(1-2), 50-58. doi:10.1159/000111499.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0010-A345-E
Abstract
B a c k g r o u n d : We have recently shown that ischemic stroke causes a stress-mediator-induced long-lasting immuno- depressive state in mice. Methods: Using head magnetic resonance imaging and standardized immunoassays, we prospectively investigated whether poststroke immuno- depression is also seen in humans. Results: Compared to healthy volunteers (n = 30), a rapid depression of lympho- cyte 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 ad- mission the combination of mono cytic tumor necrosis factor release ex vivo and the National Institute of Health Stroke Scale score were the best predictors for nosocomial infec- tion, preferentially affecting older SP. Conclusion: Our data provide evidence for an immediate suppression of cell-me- diated immune responses after ischemic stroke in humans.