title: Is the function of alveolar macrophages altered following blunt chest trauma?
abstract: OBJECTIVE
  The purpose of this study was to characterize the local pulmonary inflammatory environment and to elucidate alterations of alveolar macrophage (AMØ) functions after blunt chest trauma.
  
  
  METHODS
  Wistar rats were subjected to blunt chest trauma. AMØ were isolated, stimulated, and cultured. Bronchoalveolar lavage (BAL) was collected. Cytokines/chemokines were quantified in the BAL and in AMØ supernatants via ELISA. AMØ phagocytic and chemotactic activity and respiratory burst capacity were assessed.
  
  
  RESULTS
  Following chest trauma, a significant increase of IL-1β (at 6 and 24 h) and IL-6 (at 24 h) in BAL was observed, whereas IL-10 and TNF-α concentrations were not altered. MIP-2 and CINC were substantially increased as early as 6 h and PGE2 early at 10 min, whereas BAL MCP-1 was not elevated until 24 h after trauma. MIP-2 release by AMØ isolated form trauma animals was markedly increased as early as 10 min after injury. IL-1β and IL-10 exhibited a late increase at 24 h. AMØ TNF-α release was increased at 6 h. At 6 or 24 h, AMØ from trauma animals incorporated significantly more opsonized latex beads than their sham controls, and their chemotactic activity was substantially enhanced at 24 h. AMØ oxidative burst capacity remained largely unchanged.
  
  
  CONCLUSIONS
  Already very early after chest trauma, inflammatory mediators are present in the intraalveolar compartment. Additionally, AMØ are primed to release cytokines and chemokines. Blunt chest trauma also changes the phagocytic and chemotactic activity of AMØ. These functional changes of AMØ might enable them to better ward off potential pathogens in the course after trauma.
authors.affiliation: Department of Trauma, Hand, Plastic and Reconstructive Surgery, University of Ulm-Surgical Center, Steinhövelstraße 9, 89075 Ulm, Germany
authors.forename: Ulrich C
authors.initials: UC
authors.lastname: Liener
authors.forename: Mario
authors.initials: M
authors.lastname: Perl
authors.forename: Markus S
authors.initials: MS
authors.lastname: Huber-Lang
authors.forename: Daniel H
authors.initials: DH
authors.lastname: Seitz
authors.forename: Uwe B
authors.initials: UB
authors.lastname: Brückner
authors.forename: Florian
authors.initials: F
authors.lastname: Gebhard
authors.forename: Markus W
authors.initials: MW
authors.lastname: Knöferl
mesh_terms: D000818:Animals; D002633:Chemotaxis; D016207:Cytokines / Q000276:immunology*; D004195:Disease Models, Animal; D016676:Macrophages, Alveolar / Q000276:immunology* / Q000378:metabolism; D008297:Male; D010587:Phagocytosis; D051381:Rats; D017208:Rats, Wistar; D016897:Respiratory Burst; D013898:Thoracic Injuries / Q000276:immunology*; D014949:Wounds, Nonpenetrating / Q000276:immunology
chemical_list: D016207:Cytokines
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