Central nervous system inflammation.
Activation of inflammation is the hallmark of pathological processes that follow acute injury. This process is mediated by inflammatory cytokines and adhesion molecules that reside on the surface of endothelium, leucocyte and inflammatory cells. Attenuation of the adhesion cascade has been the subject of several basic science and clinical trials in the management of neurological injury. This review will highlight the role of adhesion molecules in the evolution of secondary injury after cerebral ischaemia and trauma. Potential therapeutic avenues will then be discussed.
Soriano
S G
SG
Harvard Medical School, Children's Hospital Boston, Perioperative and Pain Medicine, Boston, MA, USA. sulpicio.soriano@childrens.harvard.edu
Piva
S
S
D000818:Animals; D002545:Brain Ischemia / Q000473:pathology; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000378:metabolism; D002490:Central Nervous System / Q000473:pathology*; D002493:Central Nervous System Diseases / Q000473:pathology*; D018925:Chemokines / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004730:Endothelium, Vascular / Q000166:cytology; D006801:Humans; D007249:Inflammation / Q000473:pathology*; D007962:Leukocytes / Q000166:cytology; D008954:Models, Biological; D015427:Reperfusion Injury; D019087:Selectins / Q000378:metabolism
D015815:Cell Adhesion Molecules; D018925:Chemokines; D016207:Cytokines; D019087:Selectins