title: Idiopathic pneumonia after bone marrow transplantation: cytokine activation and lipopolysaccharide amplification in the bronchoalveolar compartment.
abstract: OBJECTIVE
  To determine whether idiopathic pneumonia syndrome (IPS), a form of noninfectious lung injury that follows bone marrow transplantation, is associated with cytokine activation and increased susceptibility to lipopolysaccharide (LPS).
  
  
  METHODS
  Case series.
  
  
  METHODS
  Tertiary referral center for marrow transplantation.
  
  
  METHODS
  Recipients with biopsy-confirmed IPS; normal volunteers and marrow transplant recipients without IPS were analyzed as controls.
  
  
  RESULTS
  Levels of lymphocyte and macrophage-derived cytokines as well as components of the LPS, LPS-binding protein (LBP), and CD14 system in bronchoalveolar lavage (BAL) fluid were determined. We found evidence of increased vascular permeability (BAL protein) and inflammatory cytokine activation (interleukin-1, interleukin-2, interleukin-6, and tumor necrosis factor-alpha) in patients with IPS. Patients without IPS had BAL fluid cytokine and protein levels that were similar to levels in BAL fluid from normal volunteers. Moreover, components of the LPS amplification system (LBP and soluble CD14) were increased in patients with IPS but not in patients without IPS.
  
  
  CONCLUSIONS
  These results provide direct evidence for proinflammatory cytokine activation in IPS and suggest that these patients might be at increased risk for LPS-mediated injury through the LBP amplification pathway.
authors.affiliation: Fred Hutchinson Cancer Research Center, Pulmonary and Critical Care Medicine Division, Seattle, WA 98109-1024, USA. jclark@fhcrc.org
authors.forename: J G
authors.initials: JG
authors.lastname: Clark
authors.forename: D K
authors.initials: DK
authors.lastname: Madtes
authors.forename: T R
authors.initials: TR
authors.lastname: Martin
authors.forename: R C
authors.initials: RC
authors.lastname: Hackman
authors.forename: A L
authors.initials: AL
authors.lastname: Farrand
authors.forename: S W
authors.initials: SW
authors.lastname: Crawford
mesh_terms: D000209:Acute-Phase Proteins / Q000378:metabolism; D000293:Adolescent; D000328:Adult; D016026:Bone Marrow Transplantation / Q000009:adverse effects* / Q000276:immunology; D001980:Bronchi / Q000378:metabolism*; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D002352:Carrier Proteins / Q000378:metabolism; D016022:Case-Control Studies; D016207:Cytokines / Q000378:metabolism*; D006801:Humans; D007375:Interleukin-1 / Q000378:metabolism; D007376:Interleukin-2 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D018950:Lipopolysaccharide Receptors / Q000378:metabolism; D008070:Lipopolysaccharides / Q000378:metabolism*; D008562:Membrane Glycoproteins; D008875:Middle Aged; D011014:Pneumonia / Q000209:etiology* / Q000276:immunology; D011650:Pulmonary Alveoli / Q000378:metabolism*; D016211:Transforming Growth Factor alpha / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D000099231:Lipopolysaccharide-Binding Protein
chemical_list: D000209:Acute-Phase Proteins; D002352:Carrier Proteins; D016207:Cytokines; D007375:Interleukin-1; D007376:Interleukin-2; D015850:Interleukin-6; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D016211:Transforming Growth Factor alpha; D014409:Tumor Necrosis Factor-alpha; D000099231:Lipopolysaccharide-Binding Protein