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.


METHODS
Cross-sectional study.


METHODS
Clinical research unit.


METHODS
People with SCI (N=56) and different clinical presentations, and healthy, able-bodied, age-matched control subjects (N=35).


METHODS
Not applicable.


METHODS
Serum levels of the proinflammatory cytokines interleukin (IL) 1beta, IL-6, tumor necrosis factor alpha (TNF-alpha), 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 GM(1) ganglioside (anti-GM(1)) 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-alpha, IL-1RA, and anti-GM(1) (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.
Davies
Andrew L
AL
Graduate Program in Neuroscience, London, ON, Canada; University of Western Ontario, London, ON, Canada.
Hayes
Keith C
KC
Dekaban
Gregory A
GA
D000328:Adult; D001323:Autoantibodies / Q000097:blood*; D002574:Cervical Vertebrae / Q000293:injuries; D003430:Cross-Sectional Studies; D016207:Cytokines / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005677:G(M1) Ganglioside / Q000276:immunology; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008297:Male; D018992:Myelin-Associated Glycoprotein / Q000276:immunology; D010264:Paraplegia / Q000276:immunology; D003668:Pressure Ulcer / Q000276:immunology; D011782:Quadriplegia / Q000276:immunology; D012016:Reference Values; D013119:Spinal Cord Injuries / Q000276:immunology*; D013904:Thoracic Vertebrae / Q000293:injuries; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D014552:Urinary Tract Infections / Q000276:immunology
D001323:Autoantibodies; D016207:Cytokines; D053590:Interleukin 1 Receptor Antagonist Protein; D016209:Interleukin-8; D018992:Myelin-Associated Glycoprotein; D014409:Tumor Necrosis Factor-alpha; D005677:G(M1) Ganglioside