Complement-dependent neuroinflammation in spinal cord injury: from pathology to therapeutic implications

Spinal cord injury (SCI) can cause lasting disability, and currently, only acute decompression and rehabilitation are available as treatments. Researchers are exploring the role of the complement system, which is part of the immune system, in causing inflammation in the spinal cord after an injury. The complement system can trigger and worsen inflammation in the spinal cord after an injury. This review looks at existing studies about the complement system’s role in SCI, including where the complement proteins come from, what starts their activation, and how they contribute to the damage. This review also looks at different ways to approach treatment in preclinical models of SCI and discusses the challenges of moving these treatments into use in humans. Further studies are needed to understand how different complement pathways affect SCI and to study the role of complement in white matter damage and repair.

• 1
  The complement system, a component of the innate immune system, plays a dual role in spinal cord injury (SCI), acting both as a recognition system and an immune effector, exacerbating primary injury and limiting functional recovery.
• 2
  Complement activation in SCI is triggered by factors such as direct binding to cellular debris and activation via antibody binding to damage-associated molecular patterns.
• 3
  Inhibiting specific complement components like C1q, C3, or fB results in reduced neutrophil infiltration and myeloperoxidase activity in the spinal cord, indicating a potential therapeutic strategy.