title: 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 beta2 integrins. They mediate the transmigration process of leukocytes to the abluminal side of the endothelium.
  
  
  RESULTS
  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.
authors.affiliation: Department of Neurology, University Medical Center Utrecht, Utrecht, Netherlands. C.J.M.Frijns@azu.nl
authors.forename: C J M
authors.initials: CJ
authors.lastname: Frijns
authors.forename: L J
authors.initials: LJ
authors.lastname: Kappelle
mesh_terms: D000818:Animals; D000906:Antibodies / Q000009:adverse effects / Q000627:therapeutic use; D002545:Brain Ischemia / Q000276:immunology / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000037:antagonists & inhibitors / Q000276:immunology / Q000378:metabolism*; D002561:Cerebrovascular Disorders / Q000276:immunology / Q000378:metabolism*; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000276:immunology / Q000378:metabolism*; D018799:Intercellular Adhesion Molecule-1 / Q000276:immunology / Q000378:metabolism; D007962:Leukocytes / Q000378:metabolism; D015427:Reperfusion Injury / Q000378:metabolism
chemical_list: D000906:Antibodies; D015815:Cell Adhesion Molecules; D018836:Inflammation Mediators; D018799:Intercellular Adhesion Molecule-1