Content area
Abstract
Spinal cord injury affects thousands of people every year, however, treatment options are currently limited and none are universally accepted. Inflammation has been shown to play a critical role in propagating secondary damage which exacerbates the initial trauma, therefore modulating the inflammatory response after injury has therapeutic potential. As prostaglandins are powerful inflammatory mediators in the periphery, I have examined the role of prostaglandin D 2 (PGD2) after spinal cord injury. My thesis provides evidence that PGD2 produced from hematopoietic prostaglandin D synthase plays a detrimental role in locomotor recovery. Blocking HPGDS or its receptor DP1, leads to reduced secondary damage, accompanied by changes in the immune response as well as improved locomotor recovery. My thesis provides new data about the inflammatory response that follows spinal cord injury as well as providing insight into possible therapeutic treatments for the future.
