Inappropriate Activation, Deactivation, and Probable Autooxidative Damage as a Mechanism of Neutrophil Locomotory Defect in Trauma

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Abstract
We studied 46 patients who suffered from serious blunt trauma to examine the possible mechanism of their acquired neutrophil (PMN) locomotory dysfunction. Concentrations of plasma C3adeSArg were higher in patients than in controls (310 ± 190 ng/ml vs. 90 ± 28 ng/ml, respectively; P = 3 × 10-5) . Both resting and phagocytosing PMNs from the patients produced higher quantities of H202 (0.31 × 0.29 and 5.2 × 3.4 nmol/106 PMNs per hr, respectively). These levels resemble the H 20 2 production of normal PMNs preactivated with chemotactic factor (0.85 ± 0.03 for normal and 8.2 ± 1.6 nmol/106) PMNs per hr for preactivated PMNs). Concentrations of oxidized glutathione were not significantly higher in PMNs from patients compared with PMNs from controls (0.053 ± 0.057 vs. 0.037 ± 0.046 nmol/106 PMNs, respectively; P = .5). A higher percentage of PMNs from trauma patients than from controls were capped with concanavalin A (66% ± 11% vs. 37% ± 14%, respectively; P = 4 × 10-5), a result indicating microtubular dysfunction. These findings suggest that in trauma, activation of intravascular complement results in inappropriate chemotactic stimulation and subsequent deactivation and autoxidative damage of circulating PMNs.