An optimized and validated protocol for inducing chronic experimental autoimmune encephalomyelitis in C57BL/6J mice.
Animal model
C57BL/6 mice
Experimental autoimmune encephalomyelitis
Multiple sclerosis
Myelin oligodendrocyte glycoprotein 35-55 peptide
Journal
Journal of neuroscience methods
ISSN: 1872-678X
Titre abrégé: J Neurosci Methods
Pays: Netherlands
ID NLM: 7905558
Informations de publication
Date de publication:
01 Feb 2022
01 Feb 2022
Historique:
received:
25
07
2021
revised:
10
12
2021
accepted:
12
12
2021
pubmed:
18
12
2021
medline:
1
4
2022
entrez:
17
12
2021
Statut:
ppublish
Résumé
Myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis (EAE) is the most commonly used animal model of multiple sclerosis. However, variations in the induction protocol can affect EAE progression, and may reduce the comparability of data. In the present study, we investigated the influence of the different components used for EAE induction in C57BL/6J mice on disease progression. In the present study, MOG We demonstrate that the dosage of PTx, adjusted to its potency, influences EAE development in a dose-dependent manner. Our data show that with our protocol, which considers PTx potency, C57BL/6J mice consistently develop symptoms of EAE. The mice show a typical chronic course with symptom onset after 10.5 ± 1.08 days and maximum severity around day 16 postimmunization followed by a mild remission of symptoms. Previously studies reveal that alterations in PTx dosing directly modify EAE progression. Our present study highlights that PTx batches differ in potency, resulting in inconsistent EAE induction. We also provide a clear protocol that allows a reduction in the number of mice used in EAE experiments, while maintaining consistent results. Higher standards for comparability and reproducibility are needed to ensure and maximize the generation of reliable EAE data. Specifically, consideration of PTx potency. With our method of establishing consistent EAE pathogenesis, improved animal welfare standards and a reduction of mice used in experimentation can be achieved.
Sections du résumé
BACKGROUND
BACKGROUND
Myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis (EAE) is the most commonly used animal model of multiple sclerosis. However, variations in the induction protocol can affect EAE progression, and may reduce the comparability of data.
OPTIMIZED METHOD
UNASSIGNED
In the present study, we investigated the influence of the different components used for EAE induction in C57BL/6J mice on disease progression. In the present study, MOG
RESULTS
RESULTS
We demonstrate that the dosage of PTx, adjusted to its potency, influences EAE development in a dose-dependent manner. Our data show that with our protocol, which considers PTx potency, C57BL/6J mice consistently develop symptoms of EAE. The mice show a typical chronic course with symptom onset after 10.5 ± 1.08 days and maximum severity around day 16 postimmunization followed by a mild remission of symptoms.
COMPARISON WITH EXISTING METHODS
METHODS
Previously studies reveal that alterations in PTx dosing directly modify EAE progression. Our present study highlights that PTx batches differ in potency, resulting in inconsistent EAE induction. We also provide a clear protocol that allows a reduction in the number of mice used in EAE experiments, while maintaining consistent results.
CONCLUSION
CONCLUSIONS
Higher standards for comparability and reproducibility are needed to ensure and maximize the generation of reliable EAE data. Specifically, consideration of PTx potency. With our method of establishing consistent EAE pathogenesis, improved animal welfare standards and a reduction of mice used in experimentation can be achieved.
Identifiants
pubmed: 34920025
pii: S0165-0270(21)00378-2
doi: 10.1016/j.jneumeth.2021.109443
pii:
doi:
Substances chimiques
Myelin-Oligodendrocyte Glycoprotein
0
Peptide Fragments
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
109443Informations de copyright
Copyright © 2021 The Authors. Published by Elsevier B.V. All rights reserved.