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Updated: Sep 1, 2025
Characterization and Isolation of Mouse Primary Microglia by Density Gradient Centrifugation
Published on: February 16, 2018
Central role of microglia in sepsis-associated encephalopathy: From mechanism to therapy
Xiaoqian Yan1, Kaiying Yang2, Qi Xiao2
1Department of Critical Care Medicine, The Affiliated Hospital of Qingdao University, Qingdao, China.
Abstract:
Sepsis-associated encephalopathy (SAE) is a cognitive impairment associated with sepsis that occurs in the absence of direct infection in the central nervous system or structural brain damage. Microglia are thought to be macrophages of the central nervous system, devouring bits of neuronal cells and dead cells in the brain. They are activated in various ways, and microglia-mediated neuroinflammation is characteristic of central nervous system diseases, including SAE. Here, we systematically described the pathogenesis of SAE and demonstrated that microglia are closely related to the occurrence and development of SAE. Furthermore, we comprehensively discussed the function and phenotype of microglia and summarized their activation mechanism and role in SAE pathogenesis. Finally, this review summarizes recent studies on treating cognitive impairment in SAE by blocking microglial activation and toxic factors produced after activation. We suggest that targeting microglial activation may be a putative treatment for SAE.
Insights
Sepsis-associated encephalopathy (SAE) involves cognitive impairment without direct brain infection. Targeting microglia activation offers a potential therapeutic strategy for SAE, addressing neuroinflammation and cognitive deficits.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Sepsis-associated encephalopathy (SAE) is a form of cognitive impairment linked to sepsis.
- SAE occurs without direct central nervous system (CNS) infection or structural brain damage.
- Microglia, the resident immune cells of the CNS, are implicated in SAE pathogenesis.
Purpose of the Study:
- To systematically review the pathogenesis of SAE.
- To elucidate the role of microglia in the development and progression of SAE.
- To summarize therapeutic strategies targeting microglial activation in SAE.
Main Methods:
- Systematic review of SAE pathogenesis.
- Analysis of microglial function, phenotype, and activation mechanisms.
- Review of studies investigating treatments for SAE cognitive impairment.
Main Results:
- Microglia activation and subsequent neuroinflammation are central to SAE.
- Microglial activation mechanisms and their specific roles in SAE were detailed.
- Evidence suggests blocking microglial activation can mitigate SAE-related cognitive deficits.
Conclusions:
- Microglia play a critical role in the pathogenesis of SAE.
- Targeting microglial activation presents a promising therapeutic avenue for SAE treatment.
- Further research into microglial modulation could lead to effective SAE interventions.
