title: [Ischemia and neuroimmunology--ischemia/reperfusion injury].
abstract: Immunological events are implicated in the brain damages after ischemia. Neutrophils have been implicated in the pathogenesis of ischemia-reperfusion injury. We showed beneficial effect of antineutrophol monoclonal antibody RP3, which depletes circulationing neutrophils, on brain edema formation and infarct size. In addition, marked increase in IL-8 concentration was detected in brain and serum during early reperfusion. Time course of IL-8 production precedes brain edema formation and neutrophil infiltration. It is reported that IL-1 induces IL-8 production and anti-IL-1 antibody significantly reduced ischemic brain damages. Neutralizing antibodies against cell adhesion molecules (ICAM-1 and LFA-1) regulate neutrophil: endothel adhesion and monoclonal antibodies against these adhesion molecules reduced the size of infarction. These results indicate that neutrophil infiltration into the ischemic brain is implicated in postischemic brain injury.
authors.affiliation: Department of Neurology, Tohoku University School of Medicine.
authors.forename: H
authors.initials: H
authors.lastname: Onodera
authors.forename: Y
authors.initials: Y
authors.lastname: Yamasaki
authors.forename: Y
authors.initials: Y
authors.lastname: Matsuo
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000503:physiopathology*; D015815:Cell Adhesion Molecules / Q000502:physiology; D016207:Cytokines / Q000502:physiology*; D006801:Humans; D009504:Neutrophils / Q000502:physiology; D015427:Reperfusion Injury / Q000503:physiopathology*
chemical_list: D015815:Cell Adhesion Molecules; D016207:Cytokines