title: Dendritic cells are present in ischemic brain after permanent middle cerebral artery occlusion in the rat.
abstract: OBJECTIVE
  Cerebral ischemia is associated with inflammation involving accumulation of polymorphonuclear neutrophils. T cells have been suggested to contribute to the secondary progression of ischemic brain injury. Dendritic cells (DC) are potent regulators of immunity by activating and tolerizing T cells. DC have previously been detected in rat meninges and choroid plexus. Hypothesizing that DC are involved in inflammation associated with cerebral ischemia, we investigated DC in the brain of Sprague-Dawley rats after permanent middle cerebral artery occlusion (pMCAO) versus sham operation.
  
  
  METHODS
  All experimental rats (n=24) had the right MCA permanently occluded by inserting a nylon monofilament through the right external carotid artery. Immunohistochemistry was used to detect DC (OX62(+)), microglia/macrophages (OX42(+)) that developed into DC, and activated DC expressing major histocompatibility complex class II (OX6(+)) in the brain hemispheres at 1 hour to 6 days after pMCAO or sham operation.
  
  
  RESULTS
  Levels of DC were elevated at 1 hour in the ischemic versus sham hemispheres (P<0.001) and ischemic versus nonischemic hemispheres (P<0.001). Activated DC expressing major histocompatibility complex class II (OX62(+)OX6(+)) were still elevated at 6 days after pMCAO in the ischemic versus nonischemic hemispheres (P<0.01). The area of brain lesion correlated with numbers of OX62(+) DC per 100-mm2 brain tissue section (r=0.79; P<0.0001).
  
  
  CONCLUSIONS
  Increased levels of DC in the brain after pMCAO and correlation between DC numbers and brain lesion area indicate a role for DC in cerebral ischemia. This observation could constitute a basis for further studies on the role of DC in inflammation related to cerebral ischemia.
authors.affiliation: Neuro-Angiological Research Center and Neuroimmunology Unit, Division of Neurology, Karolinska Institutet, Huddinge University Hospital, Stockholm, Sweden. Nikolaos.Kostulas@neurotec.ki.se
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Kostulas
authors.forename: Hu-Lun
authors.initials: HL
authors.lastname: Li
authors.forename: Bao-Guo
authors.initials: BG
authors.lastname: Xiao
authors.forename: Yu-Min
authors.initials: YM
authors.lastname: Huang
authors.forename: Vasilios
authors.initials: V
authors.lastname: Kostulas
authors.forename: Hans
authors.initials: H
authors.lastname: Link
mesh_terms: D000818:Animals; D000954:Antigens, Surface / Q000096:biosynthesis; D001921:Brain / Q000098:blood supply / Q000276:immunology / Q000473:pathology*; D002545:Brain Ischemia / Q000209:etiology / Q000276:immunology / Q000473:pathology*; D002452:Cell Count; D003713:Dendritic Cells / Q000473:pathology*; D004195:Disease Models, Animal; D018450:Disease Progression; D004660:Encephalitis / Q000209:etiology / Q000276:immunology / Q000473:pathology; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D020244:Infarction, Middle Cerebral Artery / Q000150:complications / Q000276:immunology / Q000473:pathology*; D007371:Interferon-gamma / Q000235:genetics / Q000378:metabolism; D007378:Interleukins / Q000235:genetics / Q000378:metabolism; D017628:Microglia / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000032:analysis / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D000954:Antigens, Surface; D007378:Interleukins; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma