Ablation of the integrin CD11b mac-1 limits deleterious responses to traumatic spinal cord injury and improves functional recovery in mice

Spinal cord injury (SCI) can lead to long-term disabilities due to a complex cascade of events including inflammation. This study investigates the role of CD11b, a protein involved in immune cell function, in this process. The researchers used mice that lacked the CD11b gene to see how its absence affected the inflammatory response and recovery after SCI. They examined various markers of inflammation and assessed the mice's motor and sensory functions. The study found that removing CD11b altered the inflammatory response, improved motor function, reduced hypersensitivity to stimuli, and limited tissue damage after SCI, suggesting CD11b plays a role in SCI pathophysiology.

• 1
  Genetic deletion of CD11b increases the neuroinflammation in the injured spinal cord tissue.
• 2
  CD11b KO mice show significantly improved locomotor functional recovery and reduced cutaneous hypersensitivity to mechanical and thermal stimuli, which were associated with reduced tissue damage.
• 3
  SCI-induced acute inflammatory response is increased, whereas production of free oxygen species in microglia/macrophages/neutrophils is reduced in the CD11b KO mice