title: Priming, second-hit priming, and apoptosis in leukocytes from trauma patients.
abstract: BACKGROUND
  Polymorphonuclear leukocytes (PMNL) play important roles in both host defenses and systemic inflammatory responses after insults. The objectives 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 trauma in seven patients. Oxidative activity, phagocytosis, and apoptosis of PMNL from serial blood samples were measured by flow cytometry. Oxidative activity with no stimulus and with formylmethionyl-leucyl-phenylalanine (FMLP) were analyzed as the priming index and FMLP response, respectively. Interleukin (IL)-6, IL-10, PMNL elastase, and thrombomodulin concentrations in blood 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 after injury. Apoptosis of PMNL was inhibited for as long as 3 weeks after injury. Infections as second hits after trauma enhanced both the priming index and the FMLP response within 24 hours after diagnosis of infection and increased serum IL-6 concentrations. However, serum thrombomodulin levels were not affected by second hits. All patients with second hits survived.
  
  
  CONCLUSIONS
  Severe trauma stimulated acute-phase priming in PMNL and inhibited apoptosis. Infections after trauma induced second-hit priming in PMNL, but the unchanged serum levels of thrombomodulin suggest that priming per se may not cause systemic vascular endothelial damage.
authors.affiliation: Department of Traumatology, Osaka University Medical School, Suita City, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Ogura
authors.forename: H
authors.initials: H
authors.lastname: Tanaka
authors.forename: T
authors.initials: T
authors.lastname: Koh
authors.forename: N
authors.initials: N
authors.lastname: Hashiguchi
authors.forename: Y
authors.initials: Y
authors.lastname: Kuwagata
authors.forename: H
authors.initials: H
authors.lastname: Hosotsubo
authors.forename: T
authors.initials: T
authors.lastname: Shimazu
authors.forename: H
authors.initials: H
authors.lastname: Sugimoto
mesh_terms: D000328:Adult; D017209:Apoptosis; D002097:C-Reactive Protein / Q000032:analysis; D005260:Female; D006801:Humans; D007239:Infections / Q000097:blood / Q000150:complications / Q000503:physiopathology; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D007958:Leukocyte Count; D019272:Leukocyte Elastase / Q000097:blood; D008297:Male; D008875:Middle Aged; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D009504:Neutrophils / Q000502:physiology*; D010587:Phagocytosis; D016897:Respiratory Burst; D013481:Superoxides / Q000378:metabolism; D018180:Thrombomodulin / Q000097:blood; D014947:Wounds and Injuries / Q000097:blood / Q000150:complications / Q000503:physiopathology*
chemical_list: D015850:Interleukin-6; D018180:Thrombomodulin; D013481:Superoxides; D016753:Interleukin-10; D009240:N-Formylmethionine Leucyl-Phenylalanine; D002097:C-Reactive Protein; D019272:Leukocyte Elastase