Neuroimmune crosstalk in chronic neuroinflammation: microglial interactions and immune modulation.
Level 5 - mechanism / opinion, no new human data
Narrative review describing mechanistic biology without systematic methodology or primary human data
PubMed 40260075 · doi:10.3389/fncel.2025.1575022
What was done
This narrative review synthesized literature on chronic central nervous system neuroinflammation, specifically examining microglial phenotypic transitions, molecular mediators (cytokines, chemokines, and extracellular vesicles), and intercellular communication with astrocytes, neurons, oligodendrocytes, and infiltrating peripheral immune cells.
What was found
The abstract reports no quantitative data or specific numerical values. It describes conceptual mechanisms wherein sustained microglial activation prompts phenotypic shifts toward neurotoxicity, drives cytokine-mediated cascades, impairs blood-brain barrier integrity, alters phagocytosis and synaptic pruning, and fuels persistent neurodegenerative cycles.
Why it matters
Mapping intercellular signaling networks and microglial phenotypic modulation highlights specific molecular pathways that could be targeted to restrain neurotoxic inflammation and restore neural homeostasis.
Limits
As a narrative review, it presents no primary clinical data, systematic search methodology, or quantitative effect sizes. Findings rely on broad mechanistic frameworks and secondary literature.
Cited by
- supports Circulating inflammatory cytokines cross the blood-brain barrier and polarize microglial cells away from supportive housekeeping states and toward destructive states.