Priming, second-hit priming, and apoptosis in leukocytes from trauma patients

Background: Polymorphonuclear leukocytes (PMNL) play important roles in bot h host defenses and systemic inflammatory responses after insults. The obje ctives of this study are to examine the serial changes in PMNL priming and apoptosis in severely injured patients and to evaluate the impact of second hits on primed PMNL function and systemic vascular endothelial damage. Methods: Twenty-four severely injured patients (mean Injury Severity Score, 31.1 +/- 9.7) were included. Infections were seen as second hits after tra uma in seven patients. Oxidative activity, phagocytosis, and apoptosis of P MNL from serial blood samples were measured by flow cytometry, Oxidative ac tivity with no stimulus and with formylmethionyl-leucyl-phenylalanine (FMLP ) were analyzed as the priming index and FMLP response, respectively. Inter leukin (IL)-6, IL-10, PMNL elastase, and thrombomodulin concentrations in b lood were also measured before and after the second hit. Results: The PMNL priming index was elevated from days 2 to 13, especially days 2 to 5 after injury. FMLP response was enhanced from days 2 to 21 afte r injury. Apoptosis of PMNL was inhibited for as long as 3 weeks after inju ry. Infections as second hits after trauma enhanced both the priming index and the FMLP response within 24 hours after diagnosis of infection and incr eased serum IL-6 concentrations. However, serum thrombomodulin levels were not affected by second hits. All patients with second hits survived. Conclusion: Severe trauma stimulated acute-phase priming in PMNL and inhibi ted apoptosis, Infections after trauma induced second-hit priming in PMNL, but the unchanged serum levels of thrombomodulin suggest that priming per s e may not cause systemic vascular endothelial damage.