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Published on: March 26, 2019
The effect of ribavirin on reactive astrogliosis in experimental autoimmune encephalomyelitis
Irena Lavrnja1, Danijela Savic, Ivana Bjelobaba
1Department of Neurobiology, Institute for Biological Research Sinisa Stankovic, University of Belgrade, Belgrade, 11060, Serbia. irenam@ibiss.bg.ac.rs
Abstract:
Experimental autoimmune encephalomyelitis (EAE) is an animal model of CNS inflammatory and demyelinating disease multiple sclerosis. Microglia and astrocytes represent two related cell types involved in the brain pathology in EAE. Accumulations of hypertrophic reactive astrocytes, intensely stained with glial fibrillary acidic protein (GFAP), which also expressed vimentin, are prominent features of EAE lesions. Recent studies from our laboratory reported that ribavirin attenuated the disease process in EAE by reducing clinical and histological manifestations. EAE was induced in genetically susceptible Dark Agouti rats with syngeneic spinal cord homogenate in complete Freund's adjuvant. Real time PCR and immunohistochemistry were used for determination of GFAP and vimentin gene and tissue expression. We have observed the increased gene and tissue expression of GFAP and vimentin in EAE rats. Ribavirin treatment significantly decreased the number of reactive astrocytes at the peak of disease. At the end of the disease, we have observed reactive GFAP(+) and vimentin(+) astrocytes in both immunized and ribavirin-treated groups, accompanied by increased level of GFAP mRNA. The present study indicates that ribavirin may have the ability to attenuate astrocyte proliferation and glial scaring at the peak of the disease and modulate the astroglial response to EAE during the time-course of the disease.
Insights
Ribavirin treatment reduced reactive astrocytes in experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. This suggests ribavirin may attenuate glial scarring and modulate the brain
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Experimental autoimmune encephalomyelitis (EAE) serves as a model for central nervous system (CNS) inflammatory and demyelinating diseases like multiple sclerosis.
- Reactive astrocytes, marked by glial fibrillary acidic protein (GFAP) and vimentin expression, are key pathological features in EAE lesions.
- Previous research indicated ribavirin's potential to reduce clinical and histological signs of EAE.
Purpose of the Study:
- To investigate the effect of ribavirin on astrocyte activation and glial scarring in EAE.
- To determine the impact of ribavirin on the gene and tissue expression of GFAP and vimentin during EAE.
Main Methods:
- EAE was induced in Dark Agouti rats using spinal cord homogenate and complete Freund's adjuvant.
- Gene and protein expression of GFAP and vimentin were analyzed using real-time PCR and immunohistochemistry.
- Ribavirin treatment was administered, and the number of reactive astrocytes was quantified.
Main Results:
- EAE induction led to increased gene and tissue expression of GFAP and vimentin.
- Ribavirin treatment significantly decreased the number of reactive astrocytes at the peak of EAE.
- Both control and ribavirin-treated groups showed reactive GFAP(+) and vimentin(+) astrocytes at the disease's end, with elevated GFAP mRNA.
Conclusions:
- Ribavirin demonstrates potential in attenuating astrocyte proliferation and glial scarring during the peak phase of EAE.
- Ribavirin may modulate the astroglial response throughout the course of experimental autoimmune encephalomyelitis.
- These findings highlight ribavirin's therapeutic possibilities in managing CNS inflammatory conditions characterized by astrogliosis.
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