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Abstract Details

Temporal and spatial patterns of inflammation and oxidative injury in human SCI
Neuro Trauma, Critical Care, and Sports Neurology
P14 - Poster Session 14 (8:00 AM-9:00 AM)
13-017

The central aim of this study is to provide an in-depth characterization of the inflammatory response and the extent of oxidative injury in traumatic human SCI.
Traumatic spinal cord injury (SCI) is a devastating condition impacting on the well-being of patients. The post-traumatic inflammatory reaction is thought to play a central role in the expansion of tissue damage in SCI. Limiting bystander damage has been proven beneficial in preclinical studies however, translation into clinical application has failed.
The study included a cohort of 23 SCI patients and 5 controls without CNS disease. Samples were collected at different time points post-injury. To characterize the origin and functional states of microglia/macrophages, the presence of lymphocyte subpopulations and the extent of oxidative injury, immunohistochemistry for various markers was performed on FFPE tissue sections.
In the SCI lesion center, microglia were diminished and lost their homeostatic phenotype. During lesion maturation, most myeloid cells in the lesions center were derived from blood-borne macrophages. They expressed a dominant pro-inflammatory phenotype and a fraction reached an intermediate (pro/anti-inflammatory) activation status. Oxidized phospholipids were initially present at increased levels in the SCI lesions center and declined over time. In contrast in the lesion rim, a substantial proportion of myeloid cells was derived from microglia. They showed a strong pro-inflammatory polarization, although in a short interval a minority of myeloid cells expressed an intermediate activation status. Oxidized phospholipids increased over time and stayed significantly elevated up to months. Overall, lymphocyte count was low and mainly consisted of CD8+ T cells. In single cases plasma cells were observed as well.
Our study provides the first systematic description of temporal and spatial patterns of inflammation and oxidative injury in human SCI. These valuable insights into the cellular composition and activation states of lesion core/rim will help to adjust future therapy designs.
Authors/Disclosures
Tobias Zrzavy
PRESENTER 		Tobias Zrzavy has nothing to disclose.
No disclosure on file
Thomas A. Berger, MD (Dept. of Neurology, Medical University of Vienna) Prof. Berger has received personal compensation in the range of $10,000-$49,999 for serving as a speaker at scientific meetings and participant of local and international advisory boards with various companies producing and markerting treatments for multiple sclerosis (Almirall, Biogen, Biologix, Bionorica, Celgene-BMS, Merck, Novartis, Roche, Sanofi-Genzyme, TG Therapeutics, UCB).
Oleg Butovsky, PhD (Brigham and Women's Hospital/Harvard Medical) No disclosure on file
No disclosure on file
Romana Hoeftberger (Medical University of Vienna) Romana Hoeftberger has received personal compensation in the range of $500-$4,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for Neurology: Neuroimmunology and Neuroinflammation. Romana Hoeftberger has received personal compensation in the range of $500-$4,999 for serving as a speaker with BMS and UCB Biopharma.