Patterns of oligodendrocyte pathology in coronavirus‐induced subacute demyelinating encephalomyelitis in the lewis rat
Identifieur interne : 001226 ( Main/Exploration ); précédent : 001225; suivant : 001227Patterns of oligodendrocyte pathology in coronavirus‐induced subacute demyelinating encephalomyelitis in the lewis rat
Auteurs : Vesna Barac-Latas [Croatie] ; Gerda Suchanek [Autriche] ; Helene Breitschopf [Autriche] ; Albert Stuehler [Allemagne] ; Helmut Wege [Allemagne] ; Hans Lassmann [Autriche]Source :
- Glia [ 0894-1491 ] ; 1997-01.
English descriptors
- Teeft :
- Acta, Acta neuropathol, Active demyelination, Apoptosis, Astrocyte, Cell death, Control tissue, Coronavirus, Coronavirus side, Demyelinated, Demyelinated plaques, Demyelinating, Demyelinating lesions, Demyelinating process, Demyelination, Different stages, Encephalomyelitis, Glial, Glial cells, Hybridization, Immune, Immunocytochemistry, Immunol, Intracerebral infection, Lassmann, Lesion, Linington, Lymphocyte, Macrophage, Mrna, Mrna expression, Multiple sclerosis, Murine, Myelin, Myelin destruction, Myelin proteins, Myelin sheaths, Neuropathol, Nuclear condensation, Oligodendrocyte, Oligodendrocyte destruction, Oligodendrocyte pathology, Plaque, Present study, Primary demyelination, Schwann cells, Sclerosis, Serial sections, Spinal cord, Virol, Virus antigen, Virus antigen expression, Virus infection, Wege, White matter, Zimprich.
Abstract
Intracerebral infection of rats with JHM coronavirus induces a chronic inflammatory demyelinating disease, which in many respects mimicks the pathology of multiple sclerosis. We investigated the patterns of demyelination and oligodendrocyte pathology in this model. In early stages of the disease infection of oligodendrocytes was associated with a downregulation of expression of mRNA for proteolipid protein in the absence of myelin destruction. When demyelinating lesions were formed infected oligodendrocytes were destroyed by necrosis, whereas oligodendrocytes that did not contain detectable virus antigen or RNA were in part dying by apoptosis. At this stage of the disease remyelination of the lesions was pronounced. At later stages after infection virus antigen was nearly completely cleared from the lesions. In spite of the lack of detectable virus, ongoing demyelination and unspecific tissue destruction occurred, and oligodendrocytes were mainly destroyed by apoptosis. These late lesions revealed only minimal central remyelination, but they were frequently repaired by Schwann cells. Our studies suggest that the mechanisms of myelin destruction in this model of virus‐induced demyelination are complex and that the patterns of tissue damage may change during the course of the disease. Glia 19:1–7, 1997 © 1997 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/(SICI)1098-1136(199701)19:1<1::AID-GLIA1>3.0.CO;2-5
Affiliations:
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demyelination</term><term>Apoptosis</term><term>Astrocyte</term><term>Cell death</term><term>Control tissue</term><term>Coronavirus</term><term>Coronavirus side</term><term>Demyelinated</term><term>Demyelinated plaques</term><term>Demyelinating</term><term>Demyelinating lesions</term><term>Demyelinating process</term><term>Demyelination</term><term>Different stages</term><term>Encephalomyelitis</term><term>Glial</term><term>Glial cells</term><term>Hybridization</term><term>Immune</term><term>Immunocytochemistry</term><term>Immunol</term><term>Intracerebral infection</term><term>Lassmann</term><term>Lesion</term><term>Linington</term><term>Lymphocyte</term><term>Macrophage</term><term>Mrna</term><term>Mrna expression</term><term>Multiple sclerosis</term><term>Murine</term><term>Myelin</term><term>Myelin destruction</term><term>Myelin proteins</term><term>Myelin sheaths</term><term>Neuropathol</term><term>Nuclear condensation</term><term>Oligodendrocyte</term><term>Oligodendrocyte destruction</term><term>Oligodendrocyte pathology</term><term>Plaque</term><term>Present study</term><term>Primary demyelination</term><term>Schwann cells</term><term>Sclerosis</term><term>Serial sections</term><term>Spinal cord</term><term>Virol</term><term>Virus antigen</term><term>Virus antigen expression</term><term>Virus infection</term><term>Wege</term><term>White matter</term><term>Zimprich</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Intracerebral infection of rats with JHM coronavirus induces a chronic inflammatory demyelinating disease, which in many respects mimicks the pathology of multiple sclerosis. We investigated the patterns of demyelination and oligodendrocyte pathology in this model. In early stages of the disease infection of oligodendrocytes was associated with a downregulation of expression of mRNA for proteolipid protein in the absence of myelin destruction. When demyelinating lesions were formed infected oligodendrocytes were destroyed by necrosis, whereas oligodendrocytes that did not contain detectable virus antigen or RNA were in part dying by apoptosis. At this stage of the disease remyelination of the lesions was pronounced. At later stages after infection virus antigen was nearly completely cleared from the lesions. In spite of the lack of detectable virus, ongoing demyelination and unspecific tissue destruction occurred, and oligodendrocytes were mainly destroyed by apoptosis. These late lesions revealed only minimal central remyelination, but they were frequently repaired by Schwann cells. Our studies suggest that the mechanisms of myelin destruction in this model of virus‐induced demyelination are complex and that the patterns of tissue damage may change during the course of the disease. Glia 19:1–7, 1997 © 1997 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>Allemagne</li><li>Autriche</li><li>Croatie</li></country><region><li>Bavière</li><li>District de Basse-Franconie</li></region><settlement><li>Wurtzbourg</li></settlement></list><tree><country name="Croatie"><noRegion><name sortKey="Barac Atas, Vesna" sort="Barac Atas, Vesna" uniqKey="Barac Atas V" first="Vesna" last="Barac-Latas">Vesna Barac-Latas</name></noRegion></country><country name="Autriche"><noRegion><name sortKey="Suchanek, Gerda" sort="Suchanek, Gerda" uniqKey="Suchanek G" first="Gerda" last="Suchanek">Gerda Suchanek</name></noRegion><name sortKey="Breitschopf, Helene" sort="Breitschopf, Helene" uniqKey="Breitschopf H" first="Helene" last="Breitschopf">Helene Breitschopf</name><name sortKey="Lassmann, Hans" sort="Lassmann, Hans" uniqKey="Lassmann H" first="Hans" last="Lassmann">Hans Lassmann</name><name sortKey="Lassmann, Hans" sort="Lassmann, Hans" uniqKey="Lassmann H" first="Hans" last="Lassmann">Hans Lassmann</name></country><country name="Allemagne"><region name="Bavière"><name sortKey="Stuehler, Albert" sort="Stuehler, Albert" uniqKey="Stuehler A" first="Albert" last="Stuehler">Albert Stuehler</name></region><name sortKey="Wege, Helmut" sort="Wege, Helmut" uniqKey="Wege H" first="Helmut" last="Wege">Helmut Wege</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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