Clinical Correlates of Elevated Serum Concentrations of Cytokines and Autoantibodies in Patients With Spinal Cord Injury

Davies AL, Hayes KC, Dekaban GA. Clinical correlates of elevated serum concentrations of cytokines and autoantibodies in patients with spinal cord injury.ObjectiveTo determine the serum cytokine profiles of patients with spinal cord injury (SCI) and varying clinical presentations relative to healthy, able-bodied, age-matched control subjects.DesignCross-sectional study.SettingClinical research unit.ParticipantsPeople with SCI (N=56) and different clinical presentations, and healthy, able-bodied, age-matched control subjects (N=35).InterventionsNot applicable.Main Outcome MeasuresSerum levels of the proinflammatory cytokines interleukin (IL) 1β, IL-6, tumor necrosis factor alpha (TNF-α), the anti-inflammatory cytokines IL-4 and IL-10, the regulatory cytokine IL-2, the IL-1 receptor antagonist (IL-1RA), and autoantibodies against myelin-associated glycoprotein and GM1 ganglioside (anti-GM1) immunoglobulin (IgG and IgM), as determined by enzyme-linked immunosorbent assay. The relationship between elevated serum cytokine levels and clinical variables was also studied.ResultsSCI subjects exhibited serum concentrations of IL-6, TNF-α, IL-1RA, and anti-GM1 (IgG) that were greater (P<.05) than control group values. Elevated cytokine concentrations were not associated with high white blood cell counts, level of injury, or American Spinal Injury Association classification; they were evident in SCI subjects who were asymptomatic for medical complications, but were further elevated in subjects with pain, urinary tract infection (UTI), and pressure ulcers.ConclusionsElevated levels of circulating proinflammatory cytokines and autoantibodies are present in the serum of SCI subjects without medical complications, and are further elevated in SCI subjects with neuropathic pain, UTI, or pressure ulcers, relative to healthy, able-bodied control subjects. These findings may be indicative of a protective autoimmunity, simply a consequence of occult or evident infection, or evidence of cytokine dysregulation that may contribute to an immune-mediated impairment of axonal conduction.