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Arterial Hypertension Aggravates Innate Immune Responses after Experimental Stroke.

Karoline Möller1, Claudia Pösel2, Alexander Kranz2

  • 1Fraunhofer Institute for Cell Therapy and Immunology Leipzig, Germany ; Institute of Anatomy, Histology and Embryology, University of Leipzig Leipzig, Germany.

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Summary

Pre-existing hypertension exacerbates stroke-induced brain inflammation, leading to larger infarct volumes in spontaneously hypertensive rats. This immune system activation explains why hypertension worsens stroke outcomes and mortality.

Keywords:
adhesion moleculesanimal modelchemokineshypertensioninflammationmacrophagesneutrophilsstroke

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Area of Science:

  • Neuroscience
  • Immunology
  • Cardiovascular Science

Background:

  • Arterial hypertension is a primary stroke risk factor, contributing to poor recovery and outcomes.
  • Hypertensive vascular remodeling worsens perfusion deficits and blood-brain barrier disruption post-stroke.
  • Pre-existing hypertension may also negatively influence post-stroke inflammation via immune system activation.

Purpose of the Study:

  • To investigate the immunological mechanisms underlying the negative impact of hypertension on stroke outcome.
  • To compare post-stroke inflammation and infarct development in hypertensive and normotensive rats.

Main Methods:

  • Male spontaneously hypertensive rats (SHRs) and Wistar Kyoto rats (WKYs) underwent photothrombotic stroke.
  • Infarct volume and functional deficits were assessed using MRI and behavioral tests.
  • Brain inflammation, leukocyte infiltration, adhesion molecule, and chemokine expression were analyzed via flow cytometry, qPCR, and immunohistochemistry.

Main Results:

  • SHRs exhibited significantly larger infarct volumes by day 3 post-stroke compared to WKYs.
  • Infarct size strongly correlated with CD45-positive leukocyte infiltration.
  • Hypertension and stroke increased chemokine expression, leading to higher monocyte, macrophage, and granulocyte infiltration in SHRs.
  • Infiltrating myeloid leukocytes in SHRs showed increased ICAM-1 expression, potentially enhancing leukocyte transmigration.

Conclusions:

  • Exacerbated brain inflammation in hypertensive rats contributes to larger infarct volumes post-stroke.
  • Increased leukocyte infiltration and adhesion molecule expression in hypertensive stroke models provide an immunological basis for poor outcomes.
  • These findings offer an immunological explanation for the epidemiological link between hypertension and adverse stroke outcomes.