title: Blunt chest trauma induces mediator-dependent monocyte migration to the lung.
abstract: OBJECTIVE
  This study was designed to determine whether lung contusion induces an increased pulmonary recruitment of monocytes as a source of alveolar macrophages and which mediators are involved.
  
  
  METHODS
  Prospective animal study.
  
  
  METHODS
  Male Sprague-Dawley rats were subjected to chest trauma by a single blast wave.
  
  
  METHODS
  Chemokine concentrations in bronchoalveolar lavage fluids and supernatants of alveolar macrophages, chemokine and chemokine receptor mRNA expressions in monocytes, pulmonary interstitial macrophages, and alveolar macrophages isolated after trauma or sham procedure were evaluated. Immigration of monocytes was determined by staining alveolar macrophages with the fluorescent marker PKH26 before chest trauma. Chemotaxis of naïve monocytes in response to bronchoalveolar lavage or supernatants from alveolar macrophages isolated after trauma or sham procedure and the migratory response of monocytes isolated after trauma/sham to recombinant chemokines were measured.
  
  
  RESULTS
  Chemokine levels in bronchoalveolar lavage and alveolar macrophage supernatants and the percentage of monocytes migrated to the lungs were increased after chest trauma. Lung contusion enhanced the mRNA expression for CCR2 in monocytes and interstitial macrophages and for monocyte chemotactic protein-1 in alveolar macrophages. Migration of naïve monocytes vs. bronchoalveolar lavage or alveolar macrophage supernatants from traumatized animals was increased when compared with samples from shams. Monocytes isolated 2 hrs after trauma showed a reduced migration to CINC-1 or monocyte chemotactic protein-1 compared with sham.
  
  
  CONCLUSIONS
  Alveolar macrophages seem to contribute to increased chemokine concentrations in alveoli of animals subjected to blunt chest trauma. Mediators released by alveolar macrophage are potent stimuli for monocyte migration. Monocytes alter their chemokine receptor expression and are recruited to the lungs.
authors.affiliation: Department of Trauma Surgery, Hand, Plastic and Reconstructive Surgery University of Ulm, Ulm, Germany.
authors.forename: Daniel H
authors.initials: DH
authors.lastname: Seitz
authors.forename: Ulrike
authors.initials: U
authors.lastname: Niesler
authors.forename: Annette
authors.initials: A
authors.lastname: Palmer
authors.forename: Michael
authors.initials: M
authors.lastname: Sulger
authors.forename: Sonja T
authors.initials: ST
authors.lastname: Braumüller
authors.forename: Mario
authors.initials: M
authors.lastname: Perl
authors.forename: Florian
authors.initials: F
authors.lastname: Gebhard
authors.forename: Markus W
authors.initials: MW
authors.lastname: Knöferl
mesh_terms: D000818:Animals; D001483:Base Sequence; D001992:Bronchoalveolar Lavage Fluid; D002465:Cell Movement; D018925:Chemokines / Q000378:metabolism; D017931:DNA Primers; D004797:Enzyme-Linked Immunosorbent Assay; D005434:Flow Cytometry; D008168:Lung / Q000276:immunology / Q000473:pathology*; D016676:Macrophages, Alveolar / Q000276:immunology; D008297:Male; D009000:Monocytes / Q000276:immunology*; D011446:Prospective Studies; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D019707:Receptors, Chemokine / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013898:Thoracic Injuries / Q000276:immunology* / Q000378:metabolism; D014949:Wounds, Nonpenetrating / Q000276:immunology* / Q000378:metabolism
chemical_list: D018925:Chemokines; D017931:DNA Primers; D012333:RNA, Messenger; D019707:Receptors, Chemokine