Stroke-induced Immunodeficiency Promotes Spontaneous Bacterial Infections and Is Mediated by Sympathetic Activation Reversal by Poststroke T Helper Cell Type 1–like Immunostimulation

• DOI: 10.1084/jem.20021098
• Publication Date: 2003-08-26T00:49:34Z
• Authors: Konstantin Prass; Christian Meisel; Conny Höflich; Johann Braun; Elke Halle; Tilo Wolf; Karsten Ruscher; Ilya V. Victorov; Josef Priller; Ulrich Dirnagl; Hans-Dieter Volk; Andreas Meisel
• Keywords: Stroke; Adoptive Cell Transfer

Infections are a leading cause of death in stroke patients. In mouse model focal cerebral ischemia, we tested the hypothesis that stroke-induced immunodeficiency increases susceptibility to bacterial infections. 3 d after all animals developed spontaneous septicemia and pneumonia. Stroke induced an extensive apoptotic loss lymphocytes shift from T helper cell (Th)1 Th2 cytokine production. Adoptive transfer natural killer cells wild-type mice, but not interferon (IFN)-γ–deficient or administration IFN-γ at day 1 greatly decreased burden. Importantly, defective response occurrence infections were prevented by blocking sympathetic nervous system hypothalamo-pituitary-adrenal axis. Furthermore, β-adrenoreceptor blocker propranolol drastically reduced mortality stroke. These data suggest catecholamine-mediated defect early lymphocyte activation is key factor impaired antibacterial immune