Homology in systemic neutrophil response induced by human experimental endotoxemia and by trauma.

The investigation of the trauma-induced innate immune responses is hampered by the wide variability in patients, type of trauma, and environmental factors. To circumvent this heterogeneity, we examined whether the systemic innate immune response toward human experimental endotoxemia is similar to the response during systemic inflammatory response syndrome after trauma. We tested the hypothesis that the innate immune response to pathogen-associated molecular pattern (e.g., lipopolysaccharides [LPSs]) and danger-associated molecular pattern (as induced by injury) leads to a comparable in vivo activation of human neutrophils. Escherichia coli LPS (2 ng/kg) was injected intravenously in nine healthy volunteers to induce a controlled systemic inflammatory response. Indices of systemic inflammation in this human inflammation model were compared with those of 12 trauma patients with a mean injury severity score of 19. Blood samples were withdrawn at 3 and 24 h after LPS-challenge or injury. Blood samples of nine healthy volunteers were used as control. Receptor expression was measured as readout for neutrophil activation by flow cytometry. Endotoxemia and injury resulted in a comparable activation phenotype of circulating neutrophils. This phenotype was characterized by downregulation of chemokine receptors CXCR1 and CXCR2 and of Fcγ receptors II and III. A significant difference between both conditions was seen in CD66b expression and for endotoxin resulted in an increased CD66b expression, whereas injury did not. Neutrophil activation was present 3 h after onset of inflammation, both during experimental endotoxemia as well as in trauma patients. Endotoxin and trauma appear to induce a similar neutrophil activation phenotype.