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Continuous cuprizone intoxication allows active experimental autoimmune encephalomyelitis induction in C57BL/6 mice.

Authors
  • Yakimov, Vladislav1, 2
  • Schweiger, Felix1, 2
  • Zhan, Jiangshan2
  • Behrangi, Newshan2
  • Horn, Anja3
  • Schmitz, Christoph1
  • Hochstrasser, Tanja1
  • Kipp, Markus4
  • 1 Institute of Anatomy II, Faculty of Medicine, LMU Munich, Pettenkoferstrasse 11, 80336, Munich, Germany. , (Germany)
  • 2 Institute of Anatomy, Rostock University Medical Center, Gertrudenstrasse 9, 18057, Rostock, Germany. , (Germany)
  • 3 Institute of Anatomy I, Faculty of Medicine, LMU Munich, Pettenkoferstrasse 11, 80336, Munich, Germany. , (Germany)
  • 4 Institute of Anatomy, Rostock University Medical Center, Gertrudenstrasse 9, 18057, Rostock, Germany. [email protected] , (Germany)
Type
Published Article
Journal
Histochemistry and cell biology
Publication Date
Aug 01, 2019
Volume
152
Issue
2
Pages
119–131
Identifiers
DOI: 10.1007/s00418-019-01786-4
PMID: 31016368
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Oligodendrocyte degeneration is a hallmark of multiple sclerosis pathology, and protecting oligodendrocytes and myelin is likely to be of clinical relevance. Traditionally, oligodendrocyte and myelin degeneration are viewed as a direct consequence of an inflammatory attack, but metabolic defects might be equally important. Appropriate animal models to study the interplay of inflammation and metabolic injury are, therefore, needed. Here, we describe that in spite of its immunosuppressive effects, a continuous intoxication with cuprizone allows the induction of active experimental autoimmune encephalomyelitis (EAE) by myelin oligodendrocyte glycoprotein (MOG35-55) immunization. Although the clinical severity of EAE is ameliorated in cuprizone-intoxicated mice, the recruitment of granulocytes, and especially, CD3+ lymphocytes into the forebrain is triggered by the cuprizone insult. Such combined lesions are further characterized by oligodendrocyte apoptosis and microglia activation, closely mimicking type III multiple sclerosis lesions. In summary, we provide a protocol that allows to study the direct interplay of immune-mediated and metabolic oligodendrocyte injury and its consequences for the cerebral white and grey matters.

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