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BioMed Research International
Volume 2013 (2013), Article ID 589048, 9 pages
http://dx.doi.org/10.1155/2013/589048
Research Article

Different Mechanisms of Inflammation Induced in Virus and Autoimmune-Mediated Models of Multiple Sclerosis in C57BL6 Mice

1Department of Biological Sciences, Indian Institute of Science Education and Research-Kolkata, Mohanpur, Nadia West Bengal 741252, India
2IISER Mohali, Knowledge City, Sector 81, SAS Nagar, Mohali 140306, India
3Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA
4Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia PA 19107, USA
5University of Pennsylvania, Scheie Eye Institute and F.M. Kirby Center for Molecular Ophthalmology, Philadelphia, PA 19104, USA

Received 7 April 2013; Accepted 1 July 2013

Academic Editor: Arianna Scuteri

Copyright © 2013 Abhinoy Kishore et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the human central nervous system (CNS). Neurotropic demyelinating strain of MHV (MHV-A59 or its isogenic recombinant strain RSA59) induces MS-like disease in mice mediated by microglia, along with a small population of T cells. The mechanism of demyelination is at least in part due to microglia-mediated myelin stripping, with some direct axonal injury. Immunization with myelin oligodendrocyte glycoprotein (MOG) induces experimental autoimmune encephalomyelitis (EAE), a mainly CD4+ T-cell-mediated disease, although CD8+ T cells may play a significant role in demyelination. It is possible that both autoimmune and nonimmune mechanisms such as direct viral toxicity may induce MS. Our study directly compares CNS pathology in autoimmune and viral-induced MS models. Mice with viral-induced and EAE demyelinating diseases demonstrated similar patterns and distributions of demyelination that accumulated over the course of the disease. However, significant differences in acute inflammation were noted. Inflammation was restricted mainly to white matter at all times in EAE, whereas inflammation initially largely involved gray matter in acute MHV-induced disease and then is subsequently localized only in white matter in the chronic disease phase. The presence of dual mechanisms of demyelination may be responsible for the failure of immunosuppression to promote long-term remission in many MS patients.