Impaired phagocytosis of Staphylococcus aureus in complete tetraplegics.

Accumulating evidence implicates the sympathetic nervous system as a modulator of immune function. Immune alteration has been observed in survivors of cervical level spinal cord injury, possibly because of dysregulation of the sympathetic outflow tracts. The majority of immune studies in the spinal cord-injured population have focused on lymphocytes. Because of the high incidence of infections in this population, we hypothesized that the immune alteration would extend to the cells of the myeloid lineage. This hypothesis was tested by analyzing the phagocytic and bactericidal function of circulating neutrophils in response to Staphylococcus aureus. A group of ten individuals with complete cervical spinal cord injury, a group of eight paraplegics with injuries below the majority of sympathetic outflow (T-10 and below), and age- and gender-matched controls for each subject were studied. In addition, a psychiatric screening for depression was completed by all subjects and controls. Paired t test revealed significantly impaired phagocytic ability in the tetraplegic group compared with their controls. The paraplegic group did not demonstrate these findings. Our results suggest that individuals who have sustained complete cervical spinal cord injury have alteration in immune function compared with neurologically intact controls, whereas those with lesions at or below T-10 do not. This in vitro finding may be related to infection after cervical spinal cord injury. The mechanism may involve dysregulation of the sympathetic arm of the autonomic nervous system.