Cellular immunodepression preceding infectious complications after acute ischemic stroke in humans

Karl Georg Haeusler1, Wolf U H Schmidt, Fabian Föhring

  • 1Berlin Neuroimaging Center and Department of Neurology, Charité - University Medicine Berlin, Berlin, Germany. georg.haeusler@charite.de

Insights

Ischemic stroke triggers immediate immune suppression in humans, impacting lymphocyte counts and immune cell function. This post-stroke immunodepression is linked to stroke severity and predicts infection risk.

Area of Science:

  • Neuroscience
  • Immunology
  • Clinical Medicine

Background:

  • Previous research indicated ischemic stroke induces a prolonged, stress-mediated immunosuppressive state in mice.
  • This study investigates the human relevance of post-stroke immunodepression.

Purpose of the Study:

  • To prospectively examine if ischemic stroke in humans leads to immune suppression.
  • To identify predictors of post-stroke complications like nosocomial infections.

Main Methods:

  • Head magnetic resonance imaging (MRI) was used to assess stroke severity.
  • Standardized immunoassays were employed to measure immune cell function (lymphocytes, monocytes, T helper type 1 cells).
  • National Institute of Health Stroke Scale (NIHSS) scores and ex vivo tumor necrosis factor alpha (TNF-α) release were analyzed.

Main Results:

  • Acute stroke patients (n=40) exhibited reduced lymphocyte counts and deactivated monocytes and T helper type 1 cells compared to healthy volunteers (n=30).
  • Immunosuppression severity correlated with clinical deficit and infarction size.
  • NIHSS score and monocytic TNF-α release predicted nosocomial infections, particularly in older patients.

Conclusions:

  • Ischemic stroke causes immediate suppression of cell-mediated immune responses in humans.
  • Post-stroke immune suppression is a significant factor influencing patient outcomes and infection risk.
Abstract

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