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Real-time Digital Imaging of Leukocyte-endothelial Interaction in Ischemia-reperfusion Injury (IRI) of the Rat Cremaster Muscle
Published on: August 5, 2012
Lymphocytic infiltration and expression of intercellular adhesion molecule-1 in photochemically induced ischemia of
S Jander1, M Kraemer, M Schroeter
1Department of Neurology, Heinrich-Heine-Universität, Düsseldorf, Germany.
Insights
The immune system contributes to ischemic stroke pathogenesis. T cells infiltrate lesions early, followed by macrophages, suggesting therapeutic targets like cell adhesion molecules for stroke treatment.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- The role of the immune system in ischemic brain damage is not fully understood.
- Investigating immune cell involvement in focal cerebral ischemia is crucial for developing new therapies.
Purpose of the Study:
- To analyze leukocyte infiltration and immune responses in a rat model of focal cerebral ischemia.
- To understand the temporal dynamics of immune cell presence and adhesion molecule expression in ischemic lesions.
Main Methods:
- Photochemically induced focal ischemia in the rat parietal cortex.
- Immunocytochemistry was used to identify and quantify infiltrating immune cells (T cells, macrophages, NK cells).
- Expression of Intercellular Adhesion Molecule-1 (ICAM-1) was assessed.
Main Results:
- T cells infiltrated ischemic lesions before macrophages, primarily in the border zone.
- Macrophage infiltration increased from day 3 to day 7, eventually clearing debris in the lesion core by day 14.
- ICAM-1 expression was observed on endothelial cells and infiltrating leukocytes during the inflammatory phase.
Conclusions:
- Ischemic lesions trigger a local immune response within the central nervous system (CNS).
- Targeting lymphocyte-derived cytokines or cell adhesion molecules like ICAM-1 may limit stroke-induced damage.
- Understanding immune cell dynamics offers potential therapeutic strategies for stroke sequelae.
Abstract:
The contribution of the immune system to the pathogenesis of ischemic lesions is still uncertain. We have analyzed leukocyte infiltration in photochemically induced focal ischemia of the rat parietal cortex by immunocytochemistry. Between 1 and 2 days after photothrombosis, CD5+ T cells adhered to subpial and cortical vessels and infiltrated the ischemic lesion prior to macrophages. By day 3 numerous T cells and some macrophages, whose number increased further between day 3 and day 7, had infiltrated the border zone around the lesion sparing the center. In addition, CD5-/CD8+ lymphocytes that probably represent natural killer cells were found. Intercellular adhesion molecule-1 (ICAM-1) was expressed on endothelial cells on days 1 and 2 and in the border zone on infiltrating leukocytes from day 3 to day 7. Starting on day 7, macrophages infiltrated the core of the lesion to remove debris. When the entire lesion was covered by macrophages at day 14, the number of T cells had decreased and ICAM-1 immunoreactivity was no longer found in or around the infarct. In conclusion, our study shows that ischemic lesions can lead to a local immune reaction in the CNS. Thus, blocking of lymphocyte-derived cytokines or cell adhesion molecules may provide a new approach to confining the sequelae of stroke.
