title: Systemic and pulmonary effector cell function after injury.
abstract: OBJECTIVE
  Traumatic injury initiates a complex inflammatory response that is associated with end-organ dysfunction, immunosuppression, and the development of nosocomial infection. We hypothesize that the lungs of injured patients experience a unique inflammatory response to traumatic injury in which the ability of alveolar effector cells to respond to a bacterial challenge is impaired.
  
  
  METHODS
  Prospective, longitudinal comparative study.
  
  
  METHODS
  The surgical intensive care unit of an ACS level I trauma center.
  
  
  METHODS
  Forty consecutive multiple trauma patients requiring mechanical ventilation.
  
  
  METHODS
  Blood and bronchoalveolar lavage fluid were collected on admission, 24, and 48 hrs postinjury. Interleukin (IL)-6, IL-8, and IL-10 were measured in each sample initially and after lipopolysaccharide stimulation by using an ex vivo model of whole blood and bronchoalveolar lavage fluid cellular contents. Five patients who underwent elective surgery formed a control group.
  
  
  RESULTS
  Systemic and alveolar levels of IL-6, IL-8, and IL-10 increase dramatically after severe injury. Levels of IL-6 and IL-8 in trauma bronchoalveolar lavage fluid are significantly greater than those of the systemic circulation. Whereas whole blood up-regulates production of IL-6 and IL-8 in response to lipopolysaccharide, bronchoalveolar lavage fluid cellular contents do not. In contrast, bronchoalveolar lavage fluid and whole blood from injured patients contain similar amounts of IL-10 and both up-regulate IL-10 production in response to lipopolysaccharide.
  
  
  CONCLUSIONS
  The lungs of injured patients experience a profound proinflammatory response to injury more severe than that of the systemic circulation. Within this setting, the ability of alveolar effector cells to respond to a bacterial challenge is diminished compared with that of systemic cells. As such, alveolar effector cell function after injury seems to be impaired, possibly explaining the high frequency of pulmonary infection among these patients.
authors.affiliation: Department of Surgery, Hennepin County Medical Center, University of Minnesota Medical School, Minneapolis, MN 55415, USA.
authors.forename: Steven G
authors.initials: SG
authors.lastname: Muehlstedt
authors.forename: Chad J
authors.initials: CJ
authors.lastname: Richardson
authors.forename: Mark
authors.initials: M
authors.lastname: Lyte
authors.forename: Jorge L
authors.initials: JL
authors.lastname: Rodriguez
mesh_terms: D000328:Adult; D001992:Bronchoalveolar Lavage Fluid; D005260:Female; D006801:Humans; D015601:Injury Severity Score; D007378:Interleukins / Q000097:blood / Q000302:isolation & purification*; D008070:Lipopolysaccharides; D008137:Longitudinal Studies; D008297:Male; D009104:Multiple Trauma / Q000097:blood / Q000145:classification / Q000503:physiopathology*; D011650:Pulmonary Alveoli / Q000378:metabolism*; D018746:Systemic Inflammatory Response Syndrome / Q000378:metabolism*
chemical_list: D007378:Interleukins; D008070:Lipopolysaccharides