Targeting the host inflammatory response in traumatic spinal cord injury.
Both acute and chronic inflammatory processes have been shown to influence outcome in experimental models of spinal cord injury. Although early inflammatory responses may participate in secondary injury processes, more delayed inflammatory events may be reparative. Therapeutic strategies that target these events are currently based on experimental findings that have clarified the cellular and molecular processes involved in the inflammatory response to injury. An increasing body of literature supports the hypothesis that acute inflammatory events are attenuated by therapeutic hypothermia and other anti-inflammatory strategies, whereas immune neuroprotection and axonal regeneration can be achieved by transfer of activated T cells or by treatment with therapeutic vaccines. These data are summarized in the present review.
Bethea
John R
JR
The Miami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami School of Medicine, Lois Pope LIFE Center, 1095 NW 14th Terrace-(R-48), Miami, FL 33136, USA. jbethea@miami.edu
Dietrich
W Dalton
WD
D000818:Animals; D006801:Humans; D007036:Hypothermia, Induced; D016753:Interleukin-10 / Q000627:therapeutic use; D009187:Myelitis / Q000276:immunology / Q000503:physiopathology / Q000628:therapy*; D009410:Nerve Degeneration / Q000276:immunology; D009416:Nerve Regeneration / Q000276:immunology; D009569:Nitric Oxide / Q000276:immunology; D013119:Spinal Cord Injuries / Q000276:immunology / Q000503:physiopathology / Q000628:therapy*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D009569:Nitric Oxide