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Updated: Jun 23, 2026
Modeling Multiple Sclerosis in the Two Sexes: MOG35-55-Induced Experimental Autoimmune Encephalomyelitis
Published on: October 13, 2023
Selective phosphodiesterase-3 inhibitor cilostazol ameliorates experimental autoimmune encephalomyelitis
Juri Kureshiro1, Katsuichi Miyamoto, Noriko Tanaka
1Department of Neurology, Kinki University School of Medicine, Ohno-higashi, Osaka-Sayama, Osaka, Japan.
Abstract:
We investigated the possible therapeutic effect of cilostazol, a specific inhibitor of phosphodiesterase-3, for experimental autoimmune encephalomyelitis (EAE). Mice affected with EAE induced by inoculation with MOG(35-55) were fed with cilostazol or vehicle control. The clinical EAE scores of the cilostazol-fed mice were lower than those of the controls. Serum level of soluble intercellular adhesion molecule-1 was significantly lower in the cilostazol-fed mice than in the controls. In the recall responses with MOG(35-55), proliferation and IFN-gamma production by lymphocytes from cilostazol-fed mice were significantly reduced. Cilostazol may exhibit repressive effects on EAE by reducing the antigen-specific T-cell response and decreasing the expression of the adhesion molecules. Cilostazol is a hopeful choice for the treatment of multiple sclerosis.
Insights
Cilostazol, a phosphodiesterase-3 inhibitor, reduced symptoms in experimental autoimmune encephalomyelitis (EAE) in mice. This suggests potential for treating multiple sclerosis by modulating T-cell responses and adhesion molecule expression.
Area of Science:
- Neuroimmunology
- Pharmacology
Background:
- Experimental autoimmune encephalomyelitis (EAE) is a model for multiple sclerosis (MS).
- Phosphodiesterase-3 (PDE3) inhibitors are being explored for various therapeutic applications.
Purpose of the Study:
- To investigate the therapeutic potential of cilostazol, a PDE3 inhibitor, in a mouse model of EAE.
- To determine cilostazol's effects on clinical symptoms, immune cell responses, and relevant molecular markers in EAE.
Main Methods:
- EAE was induced in mice using MOG(35-55) peptide.
- Mice were treated with either cilostazol or a vehicle control.
- Clinical EAE scores, serum soluble intercellular adhesion molecule-1 (sICAM-1) levels, and lymphocyte proliferation and IFN-gamma production were assessed.
Main Results:
- Cilostazol treatment significantly reduced clinical EAE scores compared to controls.
- Serum sICAM-1 levels were significantly lower in cilostazol-treated mice.
- Lymphocyte proliferation and IFN-gamma production in response to MOG(35-55) were significantly reduced by cilostazol.
Conclusions:
- Cilostazol demonstrates a therapeutic effect in EAE, likely by suppressing antigen-specific T-cell responses and reducing adhesion molecule expression.
- These findings suggest cilostazol as a promising candidate for the treatment of multiple sclerosis.
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