Increased oxidative activity in human blood neutrophils and monocytes after spinal cord injury

Traumatic injury can cause a systemic inflammatory response, increasing oxidative activity of circulating leukocytes and potentially exacerbating the original injury, as well as causing damage to initially unaffected organs. Although the importance of intraspinal inflammation after human spinal cord...

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Bibliographic Details
Published in:Experimental neurology 2009-02, Vol.215 (2), p.308-316
Main Authors: Bao, Feng, Bailey, Christopher S., Gurr, Kevin R., Bailey, Stewart I., Rosas-Arellano, M. Patricia, Dekaban, Gregory A., Weaver, Lynne C.
Format: Article
Language:English
Subjects:
Adult
Aged, 80 and over
Analysis of Variance
Biological and medical sciences
Cyclooxygenase 2 - metabolism
Female
Fluoresceins
Humans
Inflammation
Injuries of the nervous system and the skull. Diseases due to physical agents
Lipid Peroxidation - physiology
Macrophage
Male
Medical sciences
Middle Aged
Monocytes - metabolism
Neurology
Neutrophil
Neutrophils - metabolism
NF-kappa B - metabolism
Nitric Oxide Synthase Type II - metabolism
Oxidative damage
Oxidative enzyme
Peroxidase
Reactive Oxygen Species - blood
Rhodamines
Spinal Cord Injuries - blood
Trauma
Traumas. Diseases due to physical agents
Young Adult
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Summary:Traumatic injury can cause a systemic inflammatory response, increasing oxidative activity of circulating leukocytes and potentially exacerbating the original injury, as well as causing damage to initially unaffected organs. Although the importance of intraspinal inflammation after human spinal cord injury is appreciated, the role of the systemic inflammatory response to this injury is not widely recognised. We investigated oxidative activity of blood leukocytes from nine cord-injured subjects and six trauma controls (bone fractures without CNS injury) at 6 h–2 weeks after injury, comparing values to those of ten uninjured subjects. Neutrophil and monocyte free radical production, evaluated by flow cytometry, increased significantly more in cord injury subjects than in trauma controls (6-fold vs 50% increases). In leukocyte homogenates, the concentration of free radicals increased significantly more in cord injury subjects (2-fold) than in the trauma controls (1.6-fold) as did activity of myeloperoxidase (2.3-fold vs. 1.7-fold). Moreover, in homogenates and blood smears, expression of the NADPH oxidase subunit gp91 phox and of the oxidative enzyme, inducible nitric oxide synthetase was 20–25% greater in cord injury subjects than in trauma controls. Expression of the pro-inflammatory transcription factor NF-κB and of cyclooxygenase-2 increased similarly after both injuries. Finally, aldehyde products of tissue-damaging lipid peroxidation also increased significantly more in the plasma of spinal cord injury subjects than in trauma controls (2.6 fold vs. 1.9-fold). Spinal cord injury causes a particularly intense systemic inflammatory response. Limiting this response briefly after cord injury should protect the spinal cord and tissues/organs outside the CNS from secondary damage.
ISSN:0014-4886
1090-2430
DOI:10.1016/j.expneurol.2008.10.022