title: Posttraumatic auto-oxidative polymorphonuclear neutrophil receptor injury predicts the development of nosocomial infection.
abstract: OBJECTIVE
  To determine the mechanisms and prevalence of posttraumatic auto-oxidative receptor injury and immune suppression to subsequent nosocomial infections.
  
  
  METHODS
  Purified polymorphonuclear neutrophils from 30 critically ill trauma patients (mean [+/- SD] Injury Severity Scores, 21.5 +/- 7.3) were incubated with glucose and glucose-oxidase to generate superoxide anion. Subcellular fractionations were performed with iodine 1125 monoclonal antibodies against the Fc receptors CD32w and CD16 and complement receptors CD35 and CD11b/CD18. Plasma membrane expression of these receptors was then determined during the first week of hospitalization.
  
  
  METHODS
  Surgical intensive care unit in a university-affiliated hospital.
  
  
  RESULTS
  Twenty-three (77%) of 30 patients had persistent auto-oxidative reduction in Fc and complement receptors induced by glucose and glucose-oxidase. Nosocomial infections occurred in 20 (87%) of 23 patients with auto-oxidative injury vs 1 (14%) of 7 patients without auto-oxidative receptor injury (P < .01, unpaired t test). Patients without auto-oxidative injury had expression for each receptor no different from buffer control.
  
  
  CONCLUSIONS
  Critically ill trauma patients have auto-oxidative receptor injury, which is closely linked with the development of nosocomial infections. These results provide a biological basis for the early use of auto-oxidants in critically ill trauma patients.
authors.affiliation: Department of Surgery, Rhode Island Hospital/Brown University School of Medicine, Providence, USA.
authors.forename: H H
authors.initials: HH
authors.lastname: Simms
authors.forename: R
authors.initials: R
authors.lastname: D'Amico
mesh_terms: D003428:Cross Infection / Q000453:epidemiology / Q000209:etiology* / Q000276:immunology; D006801:Humans; D009504:Neutrophils / Q000276:immunology*; D018384:Oxidative Stress / Q000276:immunology*; D011951:Receptors, Complement / Q000276:immunology; D011961:Receptors, Fc / Q000276:immunology; D014947:Wounds and Injuries / Q000150:complications / Q000276:immunology*
chemical_list: D011951:Receptors, Complement; D011961:Receptors, Fc