Inflammation after spinal cord injury: a review of the critical timeline of signaling cues and cellular infiltration

Spinal cord injury (SCI) leads to loss of motor and sensory function. The initial trauma causes ischemia, oxidative damage, edema, and glutamate excitotoxicity. This starts a secondary injury cascade, which can last over 6 months, causing more cell death. Inflammation after SCI is complex, involving many cells and signaling molecules like TNFα, IL-1β, and IL-6. While inflammation has some positive effects, excessive immune cell infiltration contributes to neural degeneration. This review develops a timeline of immune cell and cytokine behavior after SCI in rodent models, highlighting differences between rats and mice. Understanding SCI pathophysiology is crucial for identifying effective therapeutic targets to reduce secondary damage.

• 1
  Proinflammatory cytokines TNFɑ, IL-1β, and IL-6 are key players early in the injury timeline, with significant upregulation within hours after SCI.
• 2
  The review highlights variations in the inflammatory response between rats and mice, particularly in anti-inflammatory cytokine regulation.
• 3
  After SCI, neutrophils enter the injured spinal cord within 6 h, but surprisingly do not reach peak numbers until 14-day post-injury and persist for up to 6-week post-injury