Neutrophil elastase mediates acute pathogenesis and is a determinant of long-term behavioral recovery after traumatic injury to the immature brain

This research explores the role of neutrophil elastase (NE), an enzyme released by immune cells, in brain injury in young mice. The study found that NE contributes to early brain damage after trauma. The researchers used genetic and drug-based methods to reduce NE activity. Reducing NE improved long-term behavioral outcomes in the injured mice. These findings suggest that targeting NE could be a potential therapeutic strategy for treating traumatic brain injury in children.

• 1
  Genetic deletion or inhibition of NE results in alleviation of acute cell death, strongly implicating NE in early post-injury pathogenesis.
• 2
  Deficits in cognitive memory and hyperactivity were markedly attenuated in brain-injured NE KO mice.
• 3
  Amelioration of brain water content in NE KO mice, despite normal neutrophil infiltration, provides evidence that NE rather than neutrophils per se directly mediates edema formation.