Inflammatory Cell Adhesion Molecules in Ischemic Cerebrovascular Disease

Abstract

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 β2 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.

Mucosal tolerance to E-selectin provides cell-mediated protection against ischemic brain injury

“…As described previously, immunomodulatory and antiinflammatory cytokine release is targeted to activated blood vessels by the E-selectin antigen specificity of regulatory T cells. This cytokine release could attenuate a variety of injury mechanisms, including effects on (i) expression of adhesion molecules (36)(37)(38)(39), (ii) activation of leukocytes (40,41), and (iii) release of proinflammatory cytokines (42,43) and many other factors involved in the pathobiology of stroke (11,12). Recent evidence also supports a role for lymphocytes in ischemic brain injury (44,45).…”

Progesterone inhibits inflammatory response pathways after permanent middle cerebral artery occlusion in rats

“…Cell adhesion molecules (CAMs) have attracted considerable attention in the study of cerebral ischemia injury (10,23,24). These adhesion molecules play an important role during stroke.…”

Optimization of time for neural stem cells transplantation for brain stroke in rats

“…Subsequent to the ischemia, as the events progress, inflammatory response causes loss of neural cells both in the center of the ischemic zone, mainly by necrosis, as well as in the penumbra, mostly by apoptosis (22,23). During acute phase, elevated levels of the otherwise lowly expressed plethora of molecules such as intercellular adhesion molecule-1 (ICAM-1), P-selectin and matrix metalloproteinases are positively correlated with clinical worsening of stroke patients thus leading to poor prognosis (24,25). Incidentally, polymorphism in MMP-9 gene and the expression of level of MMP-9 has been attributed to the risk of stroke and as a marker for the loss of blood brain barrier, edema and intensity of the inflammatory response following ischemic stroke respectively (26,27).…”