Stroke-induced Immunodeficiency Promotes Spontaneous Bacterial Infections and Is Mediated by Sympathetic Activation Reversal by Poststroke T Helper Cell Type 1–like Immunostimulation
By K. Prass, C. Meisel, C. Höflich, J. Braun, E. Halle, T. Wolf, K. Ruscher, I. Victorov, Josef Priller, U. Dirnagl and 2 more. Journal of Experimental Medicine, 2003
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Infections are a leading cause of death in stroke patients. In a mouse model of focal cerebral ischemia, we tested the hypothesis that a stroke-induced immunodeficiency increases the susceptibility to bacterial infections. 3 d after ischemia, all animals developed spontaneous septicemia and pneumonia. Stroke induced an extensive apoptotic loss of lymphocytes and a shift from T helper cell (Th)1 to Th2 cytokine production. Adoptive transfer of T and natural killer cells from wild-type mice, but not from interferon (IFN)-γ–deficient mice, or administration of IFN-γ at day 1 after stroke greatly decreased the bacterial burden. Importantly, the defective IFN-γ response and the occurrence of bacterial infections were prevented by blocking the sympathetic nervous system but not the hypothalamo-pituitary-adrenal axis. Furthermore, administration of the β-adrenoreceptor blocker propranolol drastically reduced mortality after stroke. These data suggest that a catecholamine-mediated defect in early lymphocyte activation is the key factor in the impaired antibacterial immune response after stroke.
Subfields: Biological Psychiatry, Neurology
View Paper: https://www.semanticscholar.org/paper/6345a4f2a96b71d2038864971315b7de173e6c71
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Citations in the corpus
- Guidelines for management of ischaemic stroke and transient ischaemic attack 2008. (2008, background): “A brain-mediated immunodepressive state contributes to post-stroke infection [450, 451].”
- Inflammation and Stroke: An Overview (2016, background): “Ischemic brain injury leads to sustained decrease in blood and splenic B, T, and natural killer (NK) cells in mice undergoing transient MCA occlusion [28, 31, 32].”
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- The immunology of stroke: from mechanisms to translation (2011, background): “, and steroid antagonists and the b-adrenergic receptor antagonist propanolol counteract lymphocyte apoptosis and infection propensity after stroke in rodent model”