Stroke-induced immunodeficiency promotes spontaneous bacterial infections and is mediated by sympathetic activation reversal by poststroke T helper cell Type 1-like immunostimulation

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

Research output: Contribution to journalArticlepeer-review

757 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)725-736
Number of pages12
JournalJournal of Experimental Medicine
Volume198
Issue number5
DOIs
Publication statusPublished - Sept 1 2003
Externally publishedYes

Keywords

  • Brain ischemia
  • Interferon γ
  • Natural killer cells
  • Pneumonia
  • T lymphocytes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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