Cellular immunodepression preceding infectious complications after acute ischemic stroke in humans

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