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Inflammatory cell adhesion molecules in ischemic cerebrovascular disease
1Department of Neurology, University Medical Center Utrecht, Utrecht, Netherlands. C.J.M.Frijns@azu.nl
Insights
Inflammatory cell adhesion molecules (CAMs) contribute to brain damage in stroke. While blocking CAMs reduced stroke size in animal models, this approach has not yet succeeded in human patients.
Area of Science:
- Neuroscience
- Immunology
- Vascular Biology
Background:
- Inflammatory cell adhesion molecules (CAMs) are crucial in leukocyte transmigration across the endothelium.
- Key CAMs include selectins, immunoglobulin superfamily CAMs, and beta2 integrins, expressed on endothelial cells and leukocytes.
Purpose of the Study:
- To review the role of inflammatory CAMs in ischemic stroke and delayed cerebral ischemia following subarachnoid hemorrhage.
- To explore the potential of targeting CAMs for diagnostic and therapeutic strategies in cerebrovascular disorders.
Main Methods:
- Review of existing literature on CAMs in experimental stroke models and human studies.
- Analysis of data from animal models of middle cerebral artery occlusion and subarachnoid hemorrhage.
- Examination of the effects of anti-CAM antibodies in experimental settings.
Main Results:
- CAM expression correlates with cerebral infarct size in animal stroke models.
- Absence or blockade of CAMs reduced infarct size in experimental stroke, especially with reperfusion.
- Anti-CAM treatment has not yet proven successful in human ischemic stroke patients.
- Increased CAM expression is observed in vasospastic arteries and cerebrospinal fluid following subarachnoid hemorrhage in animal models and humans.
Conclusions:
- Inflammatory CAMs are implicated in the pathogenesis of ischemic cerebrovascular disorders.
- Further research into inflammatory CAMs may yield novel diagnostic and therapeutic approaches.
- Targeting CAMs remains a potential, though currently unproven, strategy for treating stroke and related conditions.
Background:
In this review we discuss the role of inflammatory cell adhesion molecules (CAMs) in ischemic stroke and in delayed cerebral ischemia after subarachnoid hemorrhage. Vascular endothelial cells and leukocytes express several inflammatory adhesion receptors, the most important of which are the selectins, immunoglobulin gene superfamily CAMs, and beta2 integrins. They mediate the transmigration process of leukocytes to the abluminal side of the endothelium.
Summary Of Review:
There is ample evidence from animal models of middle cerebral artery occlusion that expression of CAMs is associated with cerebral infarct size. Absence of CAMs in knockout animals resulted in reduced infarct size. When middle cerebral artery occlusion in experimental stroke was followed by reperfusion, administration of anti-CAM antibodies decreased infarct size. Thus far, anti-CAM treatment has not been successful in patients with ischemic stroke. Inflammatory CAM may also play a role in the pathogenesis of delayed cerebral ischemia after subarachnoid hemorrhage. In animal models, increased expression of CAMs has been observed in vasospastic arteries. Increased concentrations of CAMs have also been found in cerebrospinal fluid of patients with subarachnoid hemorrhage.
Conclusions:
Further research on the role of inflammatory CAMs in the pathogenesis of ischemic cerebrovascular disorders should lead to new diagnostic and therapeutic strategies.