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Characterization and Isolation of Mouse Primary Microglia by Density Gradient Centrifugation
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Reprogramming microglia in sepsis-associated encephalopathy: from pathological dysfunction to therapeutic

Chen He1,2, Hui Shi2, Zhijie Yu3

  • 1Chifeng Clinical Medical College of Inner Mongolia Medical University, Chifeng, China.

Frontiers in Immunology
|May 4, 2026
PubMed
Summary

Microglia in sepsis-associated encephalopathy can shift to a harmful state. Understanding this reprogramming offers new therapeutic targets for neuroinflammation.

Keywords:
cellular reprogrammingepigenetic regulationimmune surveillanceinflammatory responsemicroglianeuroinflammationsepsis-associated encephalopathy

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Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Microglia, the CNS immune cells, are crucial in health and disease.
  • In sepsis-associated encephalopathy (SAE), microglia may transition from neuroprotective to neurotoxic phenotypes.
  • The precise mechanisms driving this microglial dysfunction in SAE are not fully understood.

Purpose of the Study:

  • To propose a framework for understanding microglial reprogramming in SAE.
  • To integrate multi-omics, genetics, and imaging data to characterize SAE-associated microglial states.
  • To identify therapeutic strategies for restoring protective microglial function.

Main Methods:

  • Review integrating single-cell multi-omics, functional genetics, and in vivo imaging.
  • Analysis of molecular characteristics and functional alterations (e.g., synaptic pruning) of microglia in SAE.
  • Discussion of inflammatory signaling, epigenetic, and metabolic factors.

Main Results:

  • Microglial dysfunction in SAE involves complex molecular and functional changes.
  • Inflammatory signals, transcriptional/epigenetic networks, and metabolic shifts are key drivers.
  • Plasticity of microglia allows for potential therapeutic modulation.

Conclusions:

  • Understanding microglial reprogramming in SAE is key to developing targeted therapies.
  • Multi-level strategies including epigenetic, metabolic, and gene-editing approaches show promise.
  • This mechanistic insight can guide interventions for various neuroinflammatory disorders.