Acceleration of superoxide production from leukocytes in trauma patients.

Superoxide (O2-) and granulocyte elastase (GE) from neutrophils mediate host defense and tissue injury in inflammation. To determine alterations in leukocyte function after trauma, O2- production and GE secretion from neutrophils were studied in trauma patients (n = 20) and healthy controls (n = 15). The priming effect of tumor necrosis factor (TNF), interleukin-1 alpha (IL-1 alpha), and lipopolysaccharide (LPS) on O2- or GE release also was evaluated. Superoxide production (nmole/10 minutes) was elevated significantly in trauma patients at days 0 (9.5 +/- 4.8), 1 (14.2 +/- 7.3), and 3 (12.2 +/- 5.9) and returned to control levels (4.2 +/- 1.6) by day 7. There was no difference in GE secretion between trauma patients and healthy controls. Incubation of neutrophils with TNF induced release of both O2- and GE. Superoxide production was induced by TNF at concentrations at or greater than 10(-11) mol/L. Granulocyte elastase secretion was induced in a time- and dose-dependent manner by TNF at concentrations between 10(-10) and 10(-7) mol/L. In contrast IL-1 alpha and LPS did not potentiate O2- or GE release. These results suggest that neutrophil O2- production increases acutely in trauma. Tumor necrosis factor may mediate this O2- and GE production by neutrophils involved in the inflammatory response.