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Drug-induced microglial phagocytosis in multiple sclerosis and experimental autoimmune encephalomyelitis and the
Wen-Yuan Ju1, Qing Wang1, Li-Juan Song1,2
1The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Research Center of Neurobiology, Shanxi University of Chinese Medicine, 030024, Taiyuan, China.
Abstract:
Microglia are resident macrophages of the central nervous system (CNS). It plays a significant role in immune surveillance under physiological conditions. On stimulation by pathogens, microglia change their phenotypes, phagocytize toxic molecules, secrete pro-inflammatory/anti-inflammatory factors, promotes tissue repair, and maintain the homeostasis in CNS. Accumulation of myelin debris in multiple sclerosis (MS)/experimental autoimmune encephalomyelitis (EAE) inhibits remyelination by decreasing the phagocytosis by microglia and prevent the recovery of MS/EAE. Drug induced microglia phagocytosis could be a novel therapeutic intervention for the treatment of MS/EAE. But the abnormal phagocytosis of neurons and synapses by activated microglia will lead to neuronal damage and degeneration. It indicates that the phagocytosis of microglia has many beneficial and harmful effects in central neurodegenerative diseases. Therefore, simply promoting or inhibiting the phagocytic activity of microglia may not achieve ideal therapeutic results. However, limited reports are available to elucidate the microglia mediated phagocytosis and its underlying molecular mechanisms. On this basis, the present review describes microglia-mediated phagocytosis, drug-induced microglia phagocytosis, molecular mechanism, and novel approach for MS/EAE treatment.
Insights
Microglia play dual roles in central nervous system diseases like multiple sclerosis (MS). Understanding their phagocytosis is key to developing new MS treatments.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Microglia are the primary immune cells of the central nervous system (CNS).
- They perform immune surveillance and maintain CNS homeostasis under physiological conditions.
- Microglia activation involves phenotypic changes, phagocytosis, and secretion of inflammatory factors.
Purpose of the Study:
- To review microglia-mediated phagocytosis in the context of central neurodegenerative diseases.
- To explore drug-induced microglia phagocytosis as a therapeutic strategy for multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE).
- To elucidate the molecular mechanisms underlying microglia phagocytosis and its dual beneficial and harmful effects.
Main Methods:
- Literature review of studies on microglia function, phagocytosis, and neuroinflammation.
- Analysis of molecular mechanisms involved in microglia-mediated phagocytosis.
- Examination of therapeutic interventions targeting microglia in MS and EAE models.
Main Results:
- Myelin debris accumulation in MS/EAE inhibits remyelination by impairing microglial phagocytosis.
- Drug-induced microglia phagocytosis shows potential for MS/EAE treatment.
- Aberrant microglial phagocytosis of neurons and synapses contributes to neurodegeneration.
Conclusions:
- Microglia-mediated phagocytosis has complex, context-dependent roles in neurodegenerative diseases.
- Targeting microglia phagocytosis requires a nuanced approach, as simple promotion or inhibition may not be optimal.
- Further research into molecular mechanisms is needed for novel therapeutic strategies in MS/EAE.
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