Comparison of Theiler's Murine Encephalomyelitis Virus Induced Spinal Cord and Peripheral Nerve Lesions Following Intracerebral and Intraspinal Infection.


Journal

International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791

Informations de publication

Date de publication:
16 Oct 2019
Historique:
received: 24 09 2019
revised: 14 10 2019
accepted: 15 10 2019
entrez: 19 10 2019
pubmed: 19 10 2019
medline: 27 2 2020
Statut: epublish

Résumé

Hallmarks of Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease (TMEV-IDD) include spinal cord (SC) inflammation, demyelination and axonal damage occurring approximately 5-8 weeks after classical intracerebral (i.c.) infection. The aim of this study was to elucidate the consequences of intraspinal (i.s.) TMEV infection and a direct comparison of classical i.c. and intraspinal infection. Swiss Jim Lambert (SJL)-mice were i.s. infected with the BeAn strain of TMEV. Clinical investigations including a scoring system and rotarod analysis were performed on a regular basis. Necropsies were performed at 3, 7, 14, 28 and 63 days post infection (dpi) following i.s. and at 4, 7, 14, 28, 56, 98, 147 and 196 dpi following i.c. infection. Serial sections of formalin-fixed, paraffin-embedded SC and peripheral nerves (PN) were investigated using hematoxylin and eosin (HE) and immunohistochemistry. I.s. infected mice developed clinical signs and a deterioration of motor coordination approximately 12 weeks earlier than i.c. infected animals. SC inflammation, demyelination and axonal damage occurred approximately 6 weeks earlier in i.s. infected animals. Interestingly, i.s. infected mice developed PN lesions, characterized by vacuolation, inflammation, demyelination and axonal damage, which was not seen following i.c. infection. The i.s. infection model offers the advantage of a significantly earlier onset of clinical signs, inflammatory and demyelinating SC lesions and additionally enables the investigation of virus-mediated PN lesions.

Identifiants

pubmed: 31623261
pii: ijms20205134
doi: 10.3390/ijms20205134
pmc: PMC6834305
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Ministry of Science and Culture of Lower Saxony
ID : Niedersachsen-Research Network on Neuroinfectiology (N-RENNT)

Déclaration de conflit d'intérêts

The authors declare no conflict of interest.

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Auteurs

Wen Jin (W)

Department of Pathology, University of Veterinary Medicine Hannover, 30559 Hannover, Germany. Wen.Jin@tiho-hannover.de.
Center for Systems Neuroscience, 30559 Hannover, Germany. Wen.Jin@tiho-hannover.de.

Eva Leitzen (E)

Department of Pathology, University of Veterinary Medicine Hannover, 30559 Hannover, Germany. Eva.Leitzen@tiho-hannover.de.
Center for Systems Neuroscience, 30559 Hannover, Germany. Eva.Leitzen@tiho-hannover.de.

Sandra Goebbels (S)

Department of Neurogenetics, Max-Planck-Institute for experimental Medicine, 37075 Göttingen, Germany. SGoebbels@em.mpg.de.

Klaus-Armin Nave (KA)

Department of Neurogenetics, Max-Planck-Institute for experimental Medicine, 37075 Göttingen, Germany. nave@em.mpg.de.

Wolfgang Baumgärtner (W)

Department of Pathology, University of Veterinary Medicine Hannover, 30559 Hannover, Germany. Wolfgang.Baumgaertner@tiho-hannover.de.
Center for Systems Neuroscience, 30559 Hannover, Germany. Wolfgang.Baumgaertner@tiho-hannover.de.

Florian Hansmann (F)

Department of Pathology, University of Veterinary Medicine Hannover, 30559 Hannover, Germany. Florian.Hansmann@tiho-hannover.de.
Center for Systems Neuroscience, 30559 Hannover, Germany. Florian.Hansmann@tiho-hannover.de.

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Classifications MeSH