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Published on: June 29, 2016
Intracellular adhesion molecule-1 and lymphocyte function-associated antigen-1 expression in a rat forebrain
1Department of Neurosurgery, Hokkaido University School of Medicine, Sapporo.
Insights
Activated leukocytes contribute to brain reperfusion injury. Increased expression of intracellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) on brain vessels and leukocytes, respectively, are observed following reperfusion.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Activated leukocytes are implicated in brain reperfusion injury.
- Intracellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) mediate leukocyte-brain interactions.
Purpose of the Study:
- To investigate the expression of ICAM-1 in cerebral vessels and LFA-1 on leukocytes after reperfusion in a rat model.
- To understand the role of these molecules in the pathophysiology of brain reperfusion injury.
Main Methods:
- A rat four-vessel occlusion model was used to induce forebrain ischemia followed by reperfusion.
- Immunohistological staining was performed to detect ICAM-1 and LFA-1 expression at various reperfusion time points (15 min to 24 hrs).
Main Results:
- ICAM-1 expression increased significantly after 1 hour of reperfusion and remained elevated on cerebral microvessels.
- LFA-1-positive leukocytes were detected in cerebral capillaries by 6 hours of reperfusion.
- Reperfusion induced increased expression of both ICAM-1 and LFA-1.
Conclusions:
- The study demonstrates that reperfusion upregulates ICAM-1 and LFA-1 expression in the rat brain.
- These molecular changes suggest a significant role for leukocyte adhesion molecules in the development of brain reperfusion injury.
Abstract:
Activated leukocytes may be involved in the reperfusion injury of the brain. The expression of intracellular adhesion molecule-1 (ICAM-1) (CD54) and lymphocyte function-associated antigen-1 (LFA-1) (CD11a/CD18) are important for the interaction of activated leukocytes with the brain. Therefore, the expression of ICAM-1 in the cerebral vessels and LFA-1 on leukocytes were examined after reperfusion in a rat four-vessel occlusion model. Model rats underwent reperfusion (15, 30, and 60 min, and 6, 12, and 24 hrs) following 30 minutes of forebrain ischemia. Immunohistological staining for ICAM-1 and LFA-1 was performed in each subgroup. ICAM-1 expression increased after 1-hour reperfusion and persisted on the cerebral microvessels in both the subcortical region and the basal ganglia. Leukocytes stained by LFA-1 were observed in the capillary vessels after 6-hour reperfusion. Increased expression of ICAM-1 and LFA-1 were induced by reperfusion, and this may be important in reperfusion injury of the brain.
