The effects of hemorrhage and trauma on interleukin 2 production

Sepsis remains the major cause of postresuscitation death after hemorrhage and trauma. The high incidence of infection in this setting has been attributed to host defense abnormalities, including dysfunction in cell-mediated immunity. To elucidate the interaction between injury and host defense mechanisms, we measured interleukin 2 (IL 2) production by peripheral blood mononuclear cells in 21 patients immediately after unanesthetized, accidental hemorrhage or trauma. Interleukin 2 production in minimally injured patients (0.63 +/- 0.14 [SEM] units) was similar to that found in control, uninjured subjects (0.68 +/- 0.17 units). Compared with control patients, IL 2 production was reduced 56% in patients with moderate injury and 85% in patients with severe injury. There was significant correlation between the severity of injury and the reduction in IL 2 production. Lymphocyte proliferative response to phytohemagglutinin was reduced in patients with moderate and severe injury, and the reduction in proliferative response was significantly correlated with injury severity. These results indicate that marked abnormalities in cell-mediated immune function, as determined by IL 2 production, occur immediately after hemorrhage and accidental injury.