Clinical Correlates of Elevated Serum Concentrations of Cytokines and Autoantibodies in Patients With Spinal Cord Injury
Abstract
Davies AL, Hayes KC, Dekaban GA. Clinical correlates of elevated serum concentrations of cytokines and autoantibodies in patients with spinal cord injury.
Objective
To 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.
Design
Cross-sectional study.
Setting
Clinical research unit.
Participants
People with SCI (N=56) and different clinical presentations, and healthy, able-bodied, age-matched control subjects (N=35).
Interventions
Not applicable.
Main Outcome Measures
Serum 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.
Results
SCI 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.
Conclusions
Elevated 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.
aGraduate Program in Neuroscience, London, ON, Canada
bDepartment of Physical Medicine & Rehabilitation, London, ON, Canada
cLawson Health Research Institute, London, ON, Canada
dDepartment of Microbiology and Immunology, London, ON, Canada
eBiotherapeutics Research Group, Robarts Research Institute, London, ON, Canada
fUniversity of Western Ontario, London, ON, Canada.
Reprint requests to Keith C. Hayes, PhD, Parkwood Hospital/SJHC, 801 Commissioners Rd E, London, ON N6C 5J1, Canada
Supported by the Parkwood Hospital Foundation and the Ontario Neurotrauma Foundation.
No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the author(s) or upon any organization with which the author(s) is/are associated.
ABSTRACT