Continuous cuprizone intoxication allows active experimental autoimmune encephalomyelitis induction in C57BL/6 mice
| Autor: | Anja K. E. Horn, Markus Kipp, Felix Schweiger, Vladislav Yakimov, Christoph Schmitz, Tanja Hochstrasser, Jiangshan Zhan, Newshan Behrangi |
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| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Histology Encephalomyelitis Autoimmune Experimental Administration Oral Inflammation Apoptosis Myelin oligodendrocyte glycoprotein 03 medical and health sciences Myelin Cuprizone Mice medicine Animals Molecular Biology Neuroinflammation 030102 biochemistry & molecular biology biology Microglia business.industry Multiple sclerosis Experimental autoimmune encephalomyelitis Cell Biology medicine.disease Oligodendrocyte Peptide Fragments Mice Inbred C57BL Medical Laboratory Technology Oligodendroglia 030104 developmental biology medicine.anatomical_structure Immunology biology.protein Female Myelin-Oligodendrocyte Glycoprotein medicine.symptom business |
| Zdroj: | Histochemistry and cell biology. 152(2) |
| ISSN: | 1432-119X |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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