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Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
Published on: May 8, 2016
Effect of viral infection on experimental allergic encephalomyelitis in mice
1Department of Medical Microbiology and Infectious Diseases, University of Alberta, Edmonton, Canada.
Abstract:
BALB/c mice were irradiated with 350 R and injected with mouse spinal cord homogenate (MSCH) in complete Freund's adjuvant. Only 15-30% of these animals developed signs of experimental allergic encephalomyelitis (EAE) at 21-28 days after inoculation. Intraperitoneal infection with the non-lethal A7 strain of Semliki forest virus (SFV) 7 days after sensitization reduced the mean appearance time of the EAE symptoms to 14 days and the number of animals with clinical EAE increased up to 70%. In contrast, virus inoculation 10 days before induction of EAE decreased significantly the incidence of clinical EAE in both BALB/c and SJL mice. Demyelination with increased cellularity, presence of macrophages, stripping of myelin from the axons and sparing of oligodendrocytes was observed in spinal cords of animals at days 13-16 after induction of EAE and subsequent virus infection. No demyelination was seen in specimens taken at the same time from mice inoculated with MSCH or SFV alone. Combined MSCH and virus inoculations induced changes in the general immune response which may be one of the major reasons for the increase or decrease in demyelination in this model.
Insights
Semliki forest virus (SFV) infection timing impacts experimental allergic encephalomyelitis (EAE) development in mice. Early SFV infection after EAE induction enhances disease, while pre-infection reduces EAE incidence and causes demyelination.
Area of Science:
- Neuroimmunology
- Virology
- Immunology
Background:
- Experimental allergic encephalomyelitis (EAE) is an autoimmune model for demyelinating diseases.
- The interplay between viral infections and autoimmune responses is complex and can influence disease pathogenesis.
Purpose of the Study:
- To investigate the effect of Semliki forest virus (SFV) infection timing on the development of EAE in mice.
- To characterize the neuropathological changes associated with combined SFV and EAE induction.
Main Methods:
- BALB/c mice were induced with EAE using mouse spinal cord homogenate (MSCH).
- Mice were infected with SFV at different time points relative to EAE induction (7 days after or 10 days before).
- Clinical EAE scoring and spinal cord histopathology were assessed.
Main Results:
- SFV infection 7 days after EAE induction increased EAE incidence and reduced symptom onset.
- SFV infection 10 days before EAE induction significantly decreased EAE incidence.
- Histopathology revealed demyelination with specific cellular changes in mice receiving combined MSCH and SFV, but not with single inoculations.
Conclusions:
- The timing of SFV infection critically modulates EAE development.
- Combined viral and autoimmune challenges induce specific demyelinating lesions.
- Altered immune responses likely mediate the observed changes in EAE incidence and severity.
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