The pathology of TBI is produced not only by the initial injury, but during the body’s protective immune response. The body’s complement system is an auxiliary, innate immune system that helps phagocytes and antibodies to clear pathogens. Unlike the adaptive immune system, the complement system is not adaptive, unable to produce counters to novel infections. In the event of traumatic brain injury, complement is a key contributor to neuropathology and disability. Deployed to the site of injury to fight infections, the complement system’s membrane attack complex (MAC) induces inflammation and inflammasome activation and causes lysis in brain cells. Thus, researchers view inhibiting MAC and preventing complement-mediated lysis as a goal in the prevention of TBI disability. The researchers sought an agent that would inhibit MAC from inducing lysis while preserving its anti-infection properties.
Published in the Proceedings of the National Academy of Sciences, an anti-complement agent that targets brain damage and promotes recovery in mice with traumatic brain injury. Crucially, the agent demonstrated effectiveness post-injury, implying the existence of a therapeutic window following head trauma for the prevention of secondary neuropathological effects and associated disability. The mice in the study demonstrated a 50 percent reduction of the neurological severity score after four hours, by comparison with untreated controls. Further, the authors note that the construct reduces inflammation, mitochondrial stress and axonal injury after incidents of TBI. By inhibiting inflammosome activation post-TBI, it regulates secondary inflammatory processes that contribute to brain injury. And importantly, as the injured mice were treated 30 minutes post-TBI, the authors suggest that a window exists for anti-complement therapy to be administered by emergency responders.
Read more at: http://medicalxpress.com/news/2015-11-effective-immune-suppression-therapy-traumatic.html