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Rapamycin combined with MCC950 to treat multiple sclerosis in experimental autoimmune encephalomyelitis
Ling Xu1,2, Cuili Zhang1, Nan Jiang3
1Department of Biotechnology, Dalian Medical University, Dalian, China.
Abstract:
Multiple sclerosis (MS) is a highly disabling demyelinating disease, which mainly affects young adults and is difficult to cure. Activated microglia may be involved in the process of neuronal cell damage and release inflammatory cytokines to injure neurons. Rapamycin (RAPA), an immunosuppressant, can induce autophagy in microglia to delay the process of the disease. As an inhibitor of NLRP3, MCC950 (CP-456773) can regulate the activation of inflammasome. An experimental autoimmune encephalomyelitis model, a disease model of MS, was established to detect the role of activated microglia in the dynamic evolution of MS. Our research showed that RAPA and MCC950 could reduce both the clinical symptom and the release of cytokines in immune cells. MCC950 reduced interleukin-1β (IL-1β) production in vivo and enhanced the effect of RAPA. We hypothesized that inflammation and demyelination in the central nervous system can be reduced by inhibiting the immune response mediated by microglia. This study provides theoretical support to the therapeutic evaluation of RAPA and MCC950 to make the mammalian targets of RAPA and NLRP3 the therapeutic targets of MS.
Insights
Rapamycin (RAPA) and MCC950 reduce multiple sclerosis (MS) symptoms by inhibiting microglial activation and inflammatory cytokine release. These findings support RAPA and MCC950 as potential therapeutic targets for MS treatment.
Area of Science:
- Neuroimmunology
- Pharmacology
Background:
- Multiple sclerosis (MS) is a debilitating demyelinating disease impacting young adults.
- Activated microglia contribute to neuronal damage and inflammation in MS.
- Current MS treatments are limited in efficacy.
Purpose of the Study:
- To investigate the therapeutic potential of Rapamycin (RAPA) and MCC950 in an experimental autoimmune encephalomyelitis (EAE) model of MS.
- To elucidate the role of activated microglia in MS pathogenesis.
- To evaluate the combined effects of RAPA and MCC950 on neuroinflammation.
Main Methods:
- Establishment of an EAE mouse model to mimic MS.
- Administration of RAPA and MCC950 to EAE mice.
- Assessment of clinical disease symptoms.
- Measurement of inflammatory cytokine release from immune cells.
Main Results:
- Both RAPA and MCC950 significantly reduced clinical symptoms in the EAE model.
- Treatment with RAPA and MCC950 decreased the release of inflammatory cytokines.
- MCC950 inhibited interleukin-1β (IL-1β) production and potentiated RAPA's effects.
Conclusions:
- Inhibition of microglial immune responses reduces central nervous system inflammation and demyelination in MS.
- RAPA and MCC950 demonstrate therapeutic promise for MS.
- Mammalian targets of RAPA (mTOR) and NLRP3 inflammasome are potential therapeutic targets for MS.
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