The effects of hemorrhage and trauma on interleukin 2 production
E. Abraham and R. F. Regan
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.
