Publisher: School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences
  • Register
  • Login

Archives of Advances in Biosciences

  • Home
  • Journal Info
    • Objectives and Scope
    • About the Journal
    • Editorial Board
    • Privacy Statement
    • Financial Policies
    • Indexing/Abstracting
    • Journal History
    • Announcements
  • Issues
    • Current
    • Archives
  • Journal Policies
    • Ethical Guidelines
    • Conflict of Interest
    • Copyright
    • Code of Publishing Ethics
    • Principles of Transparency
    • Allegations of Misconduct
    • Post-Publication Discussions and Corrections
    • Editorial Policies
    • Using Artificial Intelligence (AI)
    • Article Withdrawal
    • Complaints Process
  • Guidelines
    • Author Guidelines
    • Reviewer Guidelines
    • Journal Designer Guidelines
    • Journal Language Editor Guidelines
    • Policies of Peer Review
    • FAQ
  • Manuscript Template
    • Original Article
    • Review Article
    • Case Reports
    • Short Communication
  • Submit
  • Contact Us
Advanced Search
  1. Home
  2. Archives
  3. Vol. 12 No. 3 (2021): (summer)
  4. Research/Original Articles

Vol. 12 No. 3 (2021)

July 2021

Experimental Autoimmune Encephalomyelitis (EAE) as a Potential MS Model EAE as a Potential MS Model

  • Mohammad Hossein Gholami

Archives of Advances in Biosciences, Vol. 12 No. 3 (2021), 10 July 2021 , Page 27-40
https://doi.org/10.22037/aab.v12i3.34829 Published: 2021-07-25

  • View Article
  • Download
  • Cite
  • References
  • Statastics
  • Share

Abstract

Introduction: Multiple sclerosis (MS) is one of the most serious syndromes in human populations. Although the source of MS is unknown, some patterns have been discovered according which the genetic background and environmental factors are the key elements affecting its development. Since human samples cannot be repeatedly drawn from the spinal cord, animal models have been the best options available for studying MS so far. Experimental autoimmune encephalomyelitis (EAE) is the most recognized model in this regard. This study aimed to study EAE on rabbits to correlate symptoms and lesions, deducing whether this really can be a suitable model for predicting the algorithm lying behind the MS disease.

Materials and Methods:  For this purpose, 15 male two-month-old rabbits were divided into three groups, namely A, B, and C. The three groups were injected normal saline, complete Freund's adjuvant (CFA) + spinal cord homogenate, and normal saline + spinal cord homogenate via footpad and neck scruff, respectively. Then, they were submitted to laboratory and observed for histopathological changes.

Results: Group A did not show any signs or symptoms, while group B and C showed histopathological lesions. Moreover, group B was the only group showing clinical signs. There was also a significant difference between pathological and clinical signs in group A (p<.05), but not in group C (p>.05).

Conclusions: Considering the clinical and histopathological similarities between EAE and MS, the results suggest that EAE models are suitable to study MS.

Keywords:
  • EAE, Rabbit, MS, Animal Model, Histopathology
  • PDF

How to Cite

Gholami, M. H. (2021). Experimental Autoimmune Encephalomyelitis (EAE) as a Potential MS Model: EAE as a Potential MS Model. Archives of Advances in Biosciences, 12(3), 27–40. https://doi.org/10.22037/aab.v12i3.34829
  • ACM
  • ACS
  • APA
  • ABNT
  • Chicago
  • Harvard
  • IEEE
  • MLA
  • Turabian
  • Vancouver
  • Endnote/Zotero/Mendeley (RIS)
  • BibTeX

References

Baecher-Allan, C., B.J. Kaskow, and H.L. Weiner, Multiple sclerosis: mechanisms and immunotherapy. Neuron, 2018. 97(4): p. 742-768.

Goverman, J., Autoimmune T cell responses in the central nervous system. Nature Reviews Immunology, 2009. 9(6): p. 393-407.

Kuerten, S., K. Addicks, and P.V. Lehmann, Studies on the CNS histopathology of EAE and its correlation with clinical and immunological parameters, in Experimental Autoimmune Encephalomyelitis-Models, Disease Biology and Experimental Therapy. 2012, IntechOpen.

Hoppenbrouwers, I.A. and R.Q. Hintzen, Genetics of multiple sclerosis. Biochimica et Biophysica Acta-Molecular Basis of Disease, 2010. 1812(2): p. 194.

Oh, J., A. Vidal-Jordana, and X. Montalban, Multiple sclerosis: clinical aspects. Current opinion in neurology, 2018. 31(6): p. 752-759.

Berger, T., et al., Experimental autoimmune encephalomyelitis: the antigen specificity of T lymphocytes determines the topography of lesions in the central and peripheral nervous system. Laboratory investigation; a journal of technical methods and pathology, 1997. 76(3): p. 355-364.

Kuerten, S., et al., MP4-and MOG: 35–55-induced EAE in C57BL/6 mice differentially targets brain, spinal cord and cerebellum. Journal of neuroimmunology, 2007. 189(1-2): p. 31-40.

Longo, D.L., Daniel S. Reich, MD, Ph. D., Claudia F. Lucchinetti, MD, and Peter A. Calabresi, MD. N Engl J Med, 2018. 378: p. 169-80.

Popescu, B.F.G., I. Pirko, and C.F. Lucchinetti, Pathology of multiple sclerosis: where do we stand? CONTINUUM: Lifelong Learning in Neurology, 2013. 19(4 Multiple Sclerosis): p. 901.

Lindner, M., et al., Neurofascin 186 specific autoantibodies induce axonal injury and exacerbate disease severity in experimental autoimmune encephalomyelitis. Experimental neurology, 2013. 247: p. 259-266.

Stuart, G. and K. Krikorian, A FATAL NEURO-PARALYTIC ACCIDENT OF ANTIRABIES TREATMENT. The Lancet, 1930. 215(5569): p. 1123-1125.

Muench, G. and S.R. Robinson, Potential neurotoxic inflammatory responses to Aβ vaccination in humans. Journal of neural transmission, 2002. 109(7): p. 1081-1087.

Van Epps, H.L., Thomas Rivers and the EAE model. The Journal of experimental medicine, 2005. 202(1): p. 4.

Adelman, G., S.G. Rane, and K.F. Villa, The cost burden of multiple sclerosis in the United States: a systematic review of the literature. Journal of medical economics, 2013. 16(5): p. 639-647.

Holland, N.J., et al., Meeting the needs of people with primary progressive multiple sclerosis, their families, and the health-care community. International journal of MS care, 2011. 13(2): p. 65-74.

Jennum, P., et al., The socioeconomic consequences of multiple sclerosis: a controlled national study. European Neuropsychopharmacology, 2012. 22(1): p. 36-43.

Ortega, S.B., et al., The disease-ameliorating function of autoregulatory CD8 T cells is mediated by targeting of encephalitogenic CD4 T cells in experimental autoimmune encephalomyelitis. The Journal of Immunology, 2013. 191(1): p. 117-126.

York, N.R., et al., Immune regulatory CNS-reactive CD8+ T cells in experimental autoimmune encephalomyelitis. Journal of autoimmunity, 2010. 35(1): p. 33-44.

Sinkjér, T., et al., Non–reflex and reflex mediated ankle joint stiffness in multiple sclerosis patients with spasticity. Muscle & Nerve: Official Journal of the American Association of Electrodiagnostic Medicine, 1993. 16(1): p. 69-76.

Bielekova, B., et al., Encephalitogenic potential of the myelin basic protein peptide (amino acids 83–99) in multiple sclerosis: results of a phase II clinical trial with an altered peptide ligand. Nature medicine, 2000. 6(10): p. 1167-1175.

Kappos, L., et al., Induction of a non-encephalitogenic type 2 T helper-cell autoimmune response in multiple sclerosis after administration of an altered peptide ligand in a placebo-controlled, randomized phase II trial. Nature medicine, 2000. 6(10): p. 1176-1182.

Pedotti, R., et al., An unexpected version of horror autotoxicus: anaphylactic shock to a self-peptide. Nature immunology, 2001. 2(3): p. 216-222.

He, D., et al., Rituximab for relapsing‐remitting multiple sclerosis. Cochrane Database of Systematic Reviews, 2013(12).

Weber, M.S., et al., B‐cell activation influences T‐cell polarization and outcome of anti‐CD20 B‐cell depletion in central nervous system autoimmunity. Annals of neurology, 2010. 68(3): p. 369-383.

Morris-Downes, M.M., et al., Pathological and regulatory effects of anti-myelin antibodies in experimental allergic encephalomyelitis in mice. Journal of neuroimmunology, 2002. 125(1-2): p. 114-124.

Pedotti, R., et al., Exacerbation of experimental autoimmune encephalomyelitis by passive transfer of IgG antibodies from a multiple sclerosis patient responsive to immunoadsorption. Journal of neuroimmunology, 2013. 262(1-2): p. 19-26.

Glatigny, S. and E. Bettelli, Experimental autoimmune encephalomyelitis (EAE) as animal models of multiple sclerosis (MS). Cold Spring Harbor perspectives in medicine, 2018. 8(11): p. a028977.

Constantinescu, C.S., et al., Experimental autoimmune encephalomyelitis (EAE) as a model for multiple sclerosis (MS). British journal of pharmacology, 2011. 164(4): p. 1079-1106.

  • Abstract Viewed: 358 times
  • PDF Downloaded: 275 times

Download Statastics

  • Linkedin
  • Twitter
  • Facebook
  • Google Plus
  • Telegram

Developed By

Open Journal Systems

Information

  • For Readers
  • For Authors
  • For Librarians
  • Home
  • Archives
  • Submissions
  • About the Journal
  • Editorial Team
  • Contact

Address: P.O. Box: 19395-4618, Darband St., Qods Sq.,Tehran, Iran.

Tel: +98-21-22707346

eISSN: 2783-1264

 Archives of Advances in Biosciences is an open access article under the terms of the Creative Commons Attribution -NonCommercial 4.0 International License.( CC BY-NC 4.0)

Powered by OJSPlus