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Psychoneuroimmunology: Cardiovascular Disease

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Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain
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Published on: February 12, 2016

Beyond the usual suspects: rethinking post-stroke immunosuppression.

Laia Ascaso-Vidal1,2, Alba Simats1, David Brea1

  • 1Department of Neuroscience and Experimental Therapeutics, Instituto de Investigaciones Biomédicas de Barcelona(IIBB), Consejo Superior de Investigaciones Científicas (CSIC), Barcelona, Spain.

Frontiers in Immunology
|May 29, 2026
PubMed
Summary

Ischemic stroke triggers a biphasic immune response, leading to immunosuppression that increases infection risk. Understanding these neuroimmune interactions is crucial for improving patient outcomes after stroke.

Keywords:
ischemic strokelymphopeniaperipheral immunodepressionpost-stroke infectionsstroke-induced immunosuppression

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Last Updated: May 31, 2026

Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain
12:14

Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain

Published on: February 12, 2016

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model
08:22

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

Published on: June 20, 2025

Area of Science:

  • Neuroimmunology
  • Stroke Pathophysiology
  • Systemic Complications of Stroke

Background:

  • Ischemic stroke causes immediate injury and subsequent systemic complications.
  • A key complication is a biphasic immune response: initial inflammation followed by immunosuppression.
  • This immunosuppression elevates the risk of infections like pneumonia, increasing stroke morbidity and mortality.

Purpose of the Study:

  • To review the mechanisms driving post-stroke immunosuppression.
  • To explore the convergence and interaction of these neuroimmune pathways.
  • To discuss whether stroke-induced immunosuppression is adaptive or maladaptive.

Main Methods:

  • Literature review of current research on post-stroke immunosuppression.
  • Synthesis of findings on neuroimmune network interactions.
  • Analysis of proposed mechanisms including autonomic nervous system and HPA axis activation, DAMPs, hematopoiesis reprogramming, and neutrophil-T-cell interactions.

Main Results:

  • Stroke-induced immunosuppression is a significant factor in post-stroke complications.
  • Multiple pathways, including autonomic, endocrine, and immune system activations, contribute to this state.
  • Evidence suggests these pathways interact within a neuroimmune network.

Conclusions:

  • Post-stroke immunosuppression is a complex phenomenon driven by interacting neuroimmune mechanisms.
  • Further research is needed to determine if this state is a protective adaptation or a detrimental consequence.
  • Understanding these interactions may reveal therapeutic targets to mitigate infection risk and improve stroke recovery.