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Updated: Apr 16, 2026
A Model for Epilepsy of Infectious Etiology using Theiler's Murine Encephalomyelitis Virus
Published on: June 23, 2022
Dimethyl fumarate suppresses Theiler's murine encephalomyelitis virus-induced demyelinating disease by modifying the
Kunitoshi Kobayashi1, Hiroki Tomiki1, Yuji Inaba2
1Department of Biomedical Laboratory Sciences, Graduate School of Medicine, Matsumoto, Nagano 390-8621, Japan.
Abstract:
Dimethyl fumarate (DMF) is a modifier of the nuclear factor (erythroid-derived 2)-2 (Nrf2)-kelch-like ECH-associated protein 1 (Keap1) pathway. DMF treatment in the effector phase significantly suppressed the development of Theiler's murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD) both clinically and histologically. DMF treatment leads to an enhanced Nrf2 antioxidant response in TMEV-IDD mice. DMF treatment in the effector phase significantly suppressed the level of IL-17A mRNA. DMF is known to inhibit differentiation of T helper 17 (Th17) cells via suppressing NF-κB. Taken together, our data suggest that DMF treatment in the effector phase may suppress TMEV-IDD not only via enhancing the antioxidant response but also via suppressing IL-17A.
Insights
Dimethyl fumarate (DMF) suppresses Theiler's murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD) by enhancing antioxidant responses and reducing IL-17A. This suggests DMF is a potential therapeutic for TMEV-IDD.
Area of Science:
- Neuroimmunology
- Virology
- Pharmacology
Background:
- Theiler's murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD) is a viral model of multiple sclerosis.
- Dimethyl fumarate (DMF) modulates the Nrf2-Keap1 pathway, known for its antioxidant and anti-inflammatory roles.
Purpose of the Study:
- To investigate the therapeutic potential of DMF in the effector phase of TMEV-IDD.
- To elucidate the mechanisms underlying DMF's effects on TMEV-IDD.
Main Methods:
- Mice were infected with TMEV, and DMF treatment was initiated during the effector phase.
- Clinical and histological assessments of TMEV-IDD severity were performed.
- Nrf2 antioxidant response, IL-17A mRNA levels, and NF-κB signaling were analyzed.
Main Results:
- DMF treatment significantly suppressed clinical and histological TMEV-IDD development.
- DMF enhanced the Nrf2-mediated antioxidant response in TMEV-IDD mice.
- DMF treatment suppressed IL-17A mRNA levels and is known to inhibit Th17 differentiation via NF-κB.
Conclusions:
- DMF treatment in the effector phase offers significant protection against TMEV-IDD.
- DMF's protective effects are attributed to both enhanced antioxidant responses and suppression of IL-17A.
- DMF represents a promising therapeutic agent for TMEV-IDD by targeting multiple inflammatory pathways.
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