BACKGROUND AND PURPOSE: 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.
BACKGROUND AND PURPOSE: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: Bharti Manwani; Fudong Liu; Victoria Scranton; Matthew D Hammond; Lauren H Sansing; Louise D McCullough Journal: Exp Neurol Date: 2013-08-29 Impact factor: 5.330
Authors: Hannah X Chu; Hyun Ah Kim; Seyoung Lee; Jeffrey P Moore; Christopher T Chan; Antony Vinh; Mathias Gelderblom; Thiruma V Arumugam; Brad R S Broughton; Grant R Drummond; Christopher G Sobey Journal: J Cereb Blood Flow Metab Date: 2013-12-11 Impact factor: 6.200