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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
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The role of microglia in sepsis-associated encephalopathy: a narrative review

Le Zhang1, Mingxing Tang1, Raffaele Falsaperla2

  • 1Department of Pediatric Critical Care Medicine, Anhui Provincial Children's Hospital, Hefei, China.

Translational Pediatrics
|October 27, 2025
PubMed
Abstract

Insights

Sepsis-associated encephalopathy (SAE) involves harmful neuroinflammation driven by microglia imbalance. Targeting neuronal/glial dysfunction, circadian disruption, and the gut-brain axis offers new therapeutic avenues for SAE.

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Sepsis-associated encephalopathy (SAE) is a severe brain dysfunction characterized by neuroinflammation and blood-brain barrier (BBB) breakdown.
  • Microglial phenotypic polarization and NLRP3 inflammasome activation are central to SAE pathogenesis, creating a cycle of inflammation and neuronal damage.

Purpose of the Study:

  • To review the mechanisms of neuronal/glial dysfunction, circadian disruption, and gut-brain axis dysregulation in SAE.
  • To emphasize the interactions between these factors and microglial polarization in neuroinflammation.

Main Methods:

  • Systematic literature search in PubMed (1985-2025).
  • Keywords included "microglia", "sepsis-associated encephalopathy", "blood-brain barrier", "microglia polarization", "NLRP3 inflammasome", and "inflammation".

Main Results:

  • SAE involves complex interactions between microglial polarization, neuroinflammation, neuronal/glial dysfunction, circadian disruption, and gut-brain axis imbalance.
  • While targeting microglia shows promise, complete suppression is not advised due to their homeostatic roles.

Conclusions:

  • Future SAE therapies should balance anti-inflammatory effects with preserving microglia's reparative functions.
  • Targeting underexplored domains like circadian rhythms and the gut-brain axis is crucial for improved neuroprotection and clinical outcomes.
Keywords:
MicrogliaNLRP3 inflammasomeencephalopathyneuroinflammation

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