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(Stroke. 2002;33:1129.)
© 2002 American Heart Association, Inc.

Original Contributions

Dendritic Cells Are Present in Ischemic Brain After Permanent Middle Cerebral Artery Occlusion in the Rat

Nikolaos Kostulas, PhD; Hu-Lun Li, BSci; Bao-Guo Xiao, PhD; Yu-Min Huang, MD, PhD; Vasilios Kostulas, MD, PhD Hans Link, MD, PhD

From the Neuro-Angiological Research Center and Neuroimmunology Unit, Division of Neurology, Karolinska Institutet, Huddinge University Hospital, Stockholm, Sweden.

Correspondence to Nikolaos Kostulas, PhD, Department of Neurology, Huddinge University Hospital, S-141 86 Stockholm, Sweden. E-mail Nikolaos.Kostulas{at}neurotec.ki.se

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.

Key Words: cerebral ischemia, focal • cytokines • dendritic cells • microglia • rats

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