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The Dectin-1 Receptor Signaling Pathway Mediates the Remyelination Effect of Lentinan through Suppression of
Dandan Zhang1, Yue Jia2, Xingzong Sun1
1School of Medicine, Yunnan University, Kunming 650091, China.
Abstract:
Demyelinating diseases such as multiple sclerosis (MS) are chronic inflammatory autoimmune diseases and involve demyelination and axonal degeneration. Microglia rapidly respond to changes in the environment by altering morphotype and function during the progressive disease stage. Although substantial progress has been made in the drug development for MS, treatment of the progressive forms of the disease remains unsatisfactory. There is great interest in identifying novel agents for treating MS. Lentinus edodes is a traditional food, which can improve physiological function. Lentinan (LNT), a type of polysaccharide extracted from mushroom Lentinus edodes, is an anti-inflammatory and immunomodulatory agent. Here, we studied the remyelination effects of LNT and its therapeutic target in regulating the functions of neuroinflammation. We found that LNT enhanced remyelination and rescued motor deficiency by regulating dectin-1 receptor to inhibit neuroinflammation and microglial cell transformation. LNT promoted the conversion of microglial cells from the M1 status induced by LPS to the M2 status, enhanced the anti-inflammatory markers IL-10 and BDNF, inhibited inflammatory markers TNF-α and IL-1β, and downregulated the microglia activation and oligodendrocyte and astrocyte proliferation by modulating dectin-1. If we injected the dectin-1-specific inhibitor laminarin (Lam), the remyelination effects induced by LNT were completely abolished. Thus, these results suggest that LNT is a novel and potential therapeutic agent that can rescue MS neuroimmune imbalance and remyelination through a dectin-1 receptor-dependent mechanism.
Insights
Lentinan (LNT), a mushroom extract, promotes remyelination in multiple sclerosis (MS) by modulating microglial cells via the dectin-1 receptor. This novel therapeutic approach targets neuroinflammation and restores motor function in MS models.
Area of Science:
- Neuroimmunology
- Pharmacology
Background:
- Multiple sclerosis (MS) is a chronic inflammatory autoimmune disease characterized by demyelination and axonal degeneration.
- Current treatments for progressive MS are limited, highlighting the need for novel therapeutic agents.
- Microglia play a critical role in neuroinflammation and disease progression in MS.
Purpose of the Study:
- To investigate the remyelination effects of Lentinan (LNT), a polysaccharide from *Lentinus edodes*.
- To elucidate the therapeutic target of LNT in regulating neuroinflammation and microglial function in MS.
- To evaluate LNT's potential as a novel treatment for MS.
Main Methods:
- Assessed the effects of LNT on remyelination and motor function in an MS model.
- Investigated LNT's impact on microglial cell polarization (M1 to M2 status).
- Analyzed the expression of inflammatory and anti-inflammatory markers (TNF-α, IL-1β, IL-10, BDNF).
- Examined the role of the dectin-1 receptor by using a specific inhibitor, laminarin (Lam).
Main Results:
- LNT enhanced remyelination and rescued motor deficiency.
- LNT promoted the M2 microglial phenotype, increasing anti-inflammatory markers IL-10 and BDNF.
- LNT inhibited pro-inflammatory markers TNF-α and IL-1β, reducing microglia activation.
- Dectin-1 receptor blockade with laminarin abolished the remyelination effects of LNT.
Conclusions:
- LNT demonstrates significant remyelination potential in MS by inhibiting neuroinflammation.
- LNT acts through a dectin-1 receptor-dependent mechanism to modulate microglial function.
- LNT represents a promising therapeutic agent for addressing neuroimmune imbalance and promoting remyelination in MS.
