Metabolic Brain Disease

, Volume 27, Issue 1, pp 7–15

Myelin specific cells infiltrate MCAO lesions and exacerbate stroke severity

Authors

  • Xuefang Ren
    • Department of Anesthesiology and Perioperative MedicineOregon Health & Science University
    • Neuroimmunology Research, R&D31Portland VA Medical Center
  • Kozaburo Akiyoshi
    • Department of Anesthesiology and Perioperative MedicineOregon Health & Science University
    • Department of Anesthesiology and Critical Care MedicineKyushu University Hospital
  • Marjorie R. Grafe
    • Department of Anesthesiology and Perioperative MedicineOregon Health & Science University
    • Department of PathologyOregon Health and Science University
  • Arthur A. Vandenbark
    • Neuroimmunology Research, R&D31Portland VA Medical Center
    • Department of Veterans Affairs Medical CenterSr. Research Career Scientist, Research Service
    • Department of NeurologyOregon Health & Science University
    • Department of Molecular Microbiology & ImmunologyOregon Health & Science University
  • Patricia D. Hurn
    • Office of Health AffairsThe University of Texas System
  • Paco S. Herson
    • Department of Anesthesiology and Perioperative MedicineOregon Health & Science University
    • Department of Anesthesiology and Perioperative MedicineOregon Health & Science University
    • Neuroimmunology Research, R&D31Portland VA Medical Center
    • Department of NeurologyOregon Health & Science University
Original Paper

DOI: 10.1007/s11011-011-9267-5

Cite this article as:
Ren, X., Akiyoshi, K., Grafe, M.R. et al. Metab Brain Dis (2012) 27: 7. doi:10.1007/s11011-011-9267-5

Abstract

Although inflammatory responses increase stroke severity, the role of immune cells specific for central nervous system (CNS) antigens remains controversial. Disruption of the blood–brain barrier (BBB) during stroke allows CNS antigens to leak into the peripheral circulation and enhances access of circulating leukocytes to the brain, including those specific for CNS antigens such as myelin oligodendrocyte glycoprotein (MOG) that can induce experimental autoimmune encephalomyelitis (EAE). We here demonstrate for the first time that myelin reactive splenocytes specific for MOG transferred into severe combined immunodeficient (SCID) mice can migrate into the infarct hemisphere of recipients subjected to 60 min middle cerebral artery occlusion (MCAO) and 96 h reperfusion; moreover these cells exacerbate infarct volume and worsen neurological deficits compared to animals transferred with naïve splenocytes. These findings indicate that autoimmunity in the CNS can exert detrimental injury on brain cells and worsen the damage from ischemic stroke.

Keywords

Experimental strokeMyelin reactive splenocytesInflammatory responsesNeurologic deficit

Supplementary material

11011_2011_9267_MOESM1_ESM.docx (255 kb)
ESM 1(DOCX 254 kb)

Copyright information

© Springer Science+Business Media, LLC 2011