During bacterial, viral, or fungal infections, inflammatory signaling can extend beyond the primary site of infection and affect the central nervous system. One mechanism increasingly implicated in this process is the extracellular release of High Mobility Group Box 1 (HMGB1).
Once released from stressed or damaged cells, HMGB1 acts as a damage-associated molecular pattern (DAMP) and amplifies innate immune signaling. In the context of infection, elevated extracellular HMGB1 can contribute to:
- blood-brain barrier disruption, facilitating peripheral inflammatory signals to reach the brain
- microglial activation and pro-inflammatory polarization
- sustained neuroinflammation, even after the acute infectious phase
- neuronal structural and functional alterations associated with impaired memory, attention, and information processing
HMGB1 may actively participate in the cascade connecting peripheral infection, neuroimmune dysregulation, and cognitive decline. It could represent both a biomarker of infection-associated neuroinflammation and a therapeutic target for limiting long-term cognitive consequences.
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