title: The acute-phase response and serum amyloid A inhibit the inflammatory response to Acinetobacter baumannii Pneumonia.
abstract: BACKGROUND
  Acinetobacter baumannii is an emerging pathogen in nosocomial pneumonia. Trauma and postsurgical patients display a profound acute-phase protein response and are susceptible to pneumonia.
  
  
  METHODS
  To study the way in which the acute-phase response induced by sterile tissue injury influences pulmonary host defense, mice were injected subcutaneously with turpentine or saline in both hind limbs either 2 or 5 days before intranasal inoculation with A. baumannii.
  
  
  RESULTS
  Turpentine-injected mice demonstrated strong increases in levels of the acute-phase proteins serum amyloid A (SAA) and serum amyloid P. The inflammatory response to A. baumannii was significantly impaired in turpentine-injected mice, as shown by decreased local cytokine and chemokine levels, reduced neutrophil influx and lung myeloperoxidase activity, less pulmonary inflammation on histological examination, and lower total protein levels in their bronchoalveolar lavage fluid, which was associated with reduced bacterial clearance of A. baumannii. The late acute-phase protein response still caused lower pulmonary cytokine levels and neutrophil recruitment. Furthermore, previous injection of SAA, a major acute-phase protein, also reduced inflammatory responses to A. baumannii pneumonia.
  
  
  CONCLUSIONS
  These data suggest that the acute-phase response and SAA inhibit the local inflammatory response to A. baumannii pneumonia, which may facilitate bacterial outgrowth.
authors.affiliation: Laboratory of Experimental Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. r.renckens@amc.uva.nl
authors.forename: Rosemarijn
authors.initials: R
authors.lastname: Renckens
authors.forename: Joris J T H
authors.initials: JJ
authors.lastname: Roelofs
authors.forename: Sylvia
authors.initials: S
authors.lastname: Knapp
authors.forename: Alex F
authors.initials: AF
authors.lastname: de Vos
authors.forename: Sandrine
authors.initials: S
authors.lastname: Florquin
authors.forename: Tom
authors.initials: T
authors.lastname: van der Poll
mesh_terms: D000151:Acinetobacter Infections / Q000276:immunology* / Q000473:pathology; D040981:Acinetobacter baumannii / Q000276:immunology*; D000210:Acute-Phase Reaction / Q000276:immunology*; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D018925:Chemokines / Q000032:analysis; D003428:Cross Infection; D016207:Cytokines / Q000032:analysis; D004195:Disease Models, Animal; D006801:Humans; D007509:Irritants / Q000008:administration & dosage / Q000494:pharmacology; D008168:Lung / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D020556:Neutrophil Infiltration; D009195:Peroxidase / Q000032:analysis; D018410:Pneumonia, Bacterial / Q000276:immunology* / Q000473:pathology; D011506:Proteins / Q000032:analysis; D011994:Recombinant Proteins / Q000008:administration & dosage; D000685:Serum Amyloid A Protein / Q000008:administration & dosage / Q000502:physiology*; D014425:Turpentine / Q000008:administration & dosage / Q000494:pharmacology
chemical_list: D018925:Chemokines; D016207:Cytokines; D007509:Irritants; D011506:Proteins; D011994:Recombinant Proteins; D000685:Serum Amyloid A Protein; D009195:Peroxidase; D014425:Turpentine