4.5 Article

Elevated serum titers of proinflammatory cytokines and CNS autoantibodies in patients with chronic spinal cord injury

Journal

JOURNAL OF NEUROTRAUMA
Volume 19, Issue 6, Pages 753-761

Publisher

MARY ANN LIEBERT, INC
DOI: 10.1089/08977150260139129

Keywords

antibody; anti-GM(1); anti-MAG; autoimmune; B-lymphocyte; channelopathy; cytokine; demyelination; ganglioside; IL-2 interleukin 2; IL-4 interleukin 4; IL-10 interleukin 10; myelin-associated glycoprotein; spinal cord injury; TNF alpha (tumor necrosis factor alpha)

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This study characterized the proinflammatory cytokines, interleukin-2 (IL-2) and tumor necrosis factor alpha (TNFalpha), the antiinflammatory cytokines, IL-4 and IL-10, autoantibodies specific for GM, ganglioside (anti-GM(1)), IgG and IgM, and myelin-associated glycoprotein (anti-MAG), in the sera of infection-free, chronic (>12 months), traumatically injured SCI patients (n = 24). Healthy able-bodied subjects (n = 26) served as controls. The proinflammatory cytokines and anti-GM, antibodies were of particular interest as they have been implicated in an autoinumme channelopathy component to central and peripheral conduction deficits in various chronic neuroinflammatory diseases. Antibody and cytokine titers were established using enzyme-linked immunosorbent assays (ELISA). The mean anti-GM, (IgM) titer value for the SCI group was significantly higher (p < 0.05) than controls. The SCI group also demonstrated significantly higher titers (p < 0.05) of IL-2 and TNFa than controls. No differences were found between the SCI group and control group mean levels of IL-4 or IL-10. Overall, the serum of 57% of SCI patients contained increased levels of autoantibodies or proinflammatory cytokines relative to control values. These results provide preliminary support for the hypothesis that chronic immunological activation in the periphery occurs in a subpopulation of chronic SCI patients. It remains to be established whether elevated serum titers of proinflammatory cytokines and autoantibodies against GM, are beneficial to the patients or whether they are surrogate markers of a channelopathy that compounds the neurological impairment associated with traumatic axonopathy or myelinopathy.

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