Alterations in immune cell phenotype and function after experimental spinal cord injury

Traumatic injury to the spinal cord initiates a cascade of inflammatory-med iated injury and repair processes within the nervous system. In parallel, s pinal injury could influence peripheral mechanisms of host defense (e.g., w ound healing, antibody production) by altering lymphocyte phenotype and fun ction. The goal of this study was to evaluate the physiological impact of s pinal contusion injury on phenotypic and functional indices of lymphocyte a ctivation. A flow cytometric time-course analysis of lymphocytes isolated f rom lymph node and spleen revealed an increase in CD4(+) and a decrease in CD8(+) lymphocytes during the first week post injury. The functional potent ial of lymphocytes was also evaluated based on their ability to proliferate in the presence of a biologically relevant antigen (myelin basic protein, MBP) or a lymphocyte mitogen. The data revealed increased proliferation to MBP by 3 days postinjury in lymphocytes isolated from lymph node but not sp leen. By 1 week postinjury, increased proliferation to mitogen was noted in both the lymph node and the spleen suggesting a general increase in lympho cyte reactivity during this time interval. Circulating corticosterone (CORT ), an endogenous glucocorticoid with significant effects on lymphocyte phen otype and function, was elevated within 24 h after spinal cord injury (SCI) and remained above control levels throughout the duration of our studies ( up to 1 month postinjury). The present data suggest injury-associated chang es in immune cell phenotype and function paralleled by the activation of th e hypothalamic-pituitary-adrenal (HPA) axis.