High mobility group box-1 protein promotes astrocytic CCL5 production through the MAPK/NF-κB pathway following spinal cord injury

Astrocytes, acting as immune cells, produce chemokines that attract leukocytes to the injury site after spinal cord injury (SCI), contributing to inflammation. The study found that HMGB1, a protein released after SCI, correlates with increased CCL5, a chemokine, in astrocytes. Inhibiting HMGB1 reduces CCL5 production, decreasing inflammatory cell recruitment and improving motor function recovery after SCI.

• 1
  SCI increases CCL5 and HMGB1 protein levels synchronously at the lesion site.
• 2
  HMGB1 facilitates CCL5 production in astrocytes via TLR2/4 receptors and the ERK/JNK-mediated NF-κB pathway.
• 3
  HMGB1-mediated astrocytic CCL5 expression promotes microglia/macrophage migration and M1 polarization.