Posttraumatic Inflammation as a Key to Neuroregeneration after Traumatic Spinal Cord Injury

Abstract

Pro- and anti-inflammatory cytokines might have a large impact on the secondary phase and on the neurological outcome of patients with acute spinal cord injury (SCI). We measured the serum levels of different cytokines (Interferon-γ, Tumor Necrosis Factor-α, Interleukin-1β, IL-6, IL-8, IL-10, and Vascular Endothelial Growth Factor) over a 12-week period in 40 acute traumatic SCI patients: at admission on average one hour after initial trauma; at four, nine, 12, and 24 h; Three, and seven days after admission; and two, four, eight, and twelve weeks after admission. This was done using a Luminex Performance Human High Sensitivity Cytokine Panel. SCI was classified using the American Spinal Injury Association (ASIA) Impairment Scale (AIS) at time of admission and after 12 weeks. TNFα, IL-1β, IL-6, IL-8, and IL-10 concentrations were significantly higher in patients without neurological remission and in patients with an initial AIS A (p < 0.05). This study shows significant differences in cytokine concentrations shown in traumatic SCI patients with different neurological impairments and within a 12-week period. IL-8 and IL-10 are potential peripheral markers for neurological remission and rehabilitation after traumatic SCI. Furthermore our cytokine expression pattern of the acute, subacute, and intermediate phase of SCI establishes a possible basis for future studies to develop standardized monitoring, prognostic, and tracking techniques.

Bone marrow mesenchymal stem cells stimulated with low‐intensity pulsed ultrasound: Better choice of transplantation treatment for spinal cord injury

“…The pathology of SCI can be characterized by two phases of lesions: the primary lesion involves mechanical damage of the spinal cord relevant to hemorrhage, electrolyte flow and the release of lysosomes and other cellular components. The secondary lesion includes edema, ischemia, inflammation reactions, ionic imbalance (eg, intracellular calcium), excitotoxicity, caspase and calpain activation, neurotransmitter accumulation, and apoptosis . The subacute stage of SCI is known to be deleterious for axonal regeneration and functional recovery.…”

“…The secondary lesion includes edema, ischemia, inflammation reactions, ionic imbalance (eg, intracellular calcium), excitotoxicity, caspase and calpain activation, neurotransmitter accumulation, and apoptosis. 3,4 The subacute stage of SCI is known to be deleterious for axonal regeneration and functional recovery. This indicates that spontaneous recovery occurs in a limited time window.…”

sCD95L in serum after spinal cord injury

“…Further, we were able to demonstrate that proand anti-inflammatory cytokines might have a key role by inducing and controlling these feedback loops after SCI. 9 However, there is still an ongoing discussion about inflammation and its influence on neuro de-and regeneration. In general, inflammation needs to be controlled in order to avoid additional damage by disproportionate defense mechanisms, but it is also essential for responding to external noxae such as bacterial or viral wound infections, as well as putting important repair mechanisms in motion.…”

“…Two dependent variables (cytokine concentrations within one group at different points of time) were compared with the Wilcoxon signed-rank test. 9 Our prospective observational study has been approved by the ethics committees of the University of Heidelberg (S-514/2011) and the Landesärztekammer Rheinland-Pfalz (837.188.12/8289-F), Germany. We certify that all applicable institutional and governmental regulations concerning the ethical use of human volunteers were followed during the course of this research.…”

“…9 We defined neurological remission as improvement of the final AIS score compared with the initially measured AIS score. Finally, we divided patients according to their neurological outcome into two groups: G1, patients with neurological remission (G1 = Group 1, improved the final AIS score compared with the initial AIS score), and G2, patients without remission (G2 = Group 2, no improvement in the final AIS score compared with the initial AIS score).…”