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Endothelial ICAM-1 expression associated with inflammatory cell response in human ischemic stroke
P J Lindsberg1, O Carpén, A Paetau
1Department of Neurology, University of Helsinki, Finland.
Circulation
|September 1, 1996
Summary
Leukocyte infiltration in the brain after stroke is linked to increased intercellular adhesion molecule-1 (ICAM-1) expression. Blocking ICAM-1 may reduce stroke-related damage.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Leukocyte adhesion to endothelium post-ischemia may worsen brain injury.
- Mechanisms of cerebral leukocyte infiltration and therapeutic targets in humans remain unclear.
Purpose of the Study:
- To investigate cerebral leukocyte infiltration and endothelial adhesion molecule expression in human stroke patients.
Main Methods:
- Immunohistochemistry was used to analyze brain sections from stroke victims (15 hours to 18 days post-stroke) and controls.
- Quantification of granulocytes, mononuclear phagocytes, and microvessels expressing intercellular adhesion molecule-1 (ICAM-1).
Main Results:
- Granulocytes infiltrated infarcted regions within 15 hours, peaking by 2.2 days.
- Acute infarctions showed significantly higher ICAM-1 expression in microvessels compared to noninfarcted hemispheres and controls.
- Macrophages were abundant in neuronal damage cores later (17-18 days) in the absence of ICAM-1 upregulation.
Conclusions:
- Upregulation of endothelial ICAM-1 likely drives granulocyte infiltration in the initial days after stroke.
- Targeting endothelial adhesion molecules, such as ICAM-1, may offer therapeutic benefits for reducing leukocyte-induced stroke damage.