title: Neutrophil inflammation and activation in bronchiectasis: comparison with pneumonia and idiopathic pulmonary fibrosis.
abstract: BACKGROUND
  Pulmonary inflammation in bronchiectasis, pneumonia and idiopathic pulmonary fibrosis (IPF) is dominated by neutrophils. Pathophysiologic differences are seen in the degree of airway and tissue destruction. Neutrophil activation and neutrophil proteolytic activity might differ between bronchiectasis, pneumonia and IPF.
  
  
  OBJECTIVE
  The aim of this study was to determine whether levels of inflammatory and protective markers in bronchoalveolar lavage (BAL) differed among cases of bronchiectasis, pneumonia and IPF.
  
  
  METHODS
  We studied 11 bronchiectasis patients (group 1), 30 pneumonia patients (group 2), 15 IPF patients (group 3) and 12 healthy volunteers (group 4). In the bronchoalveolar lavage fluid, concentrations of alpha(1)-proteinase inhibitor, myeloperoxidase (MPO) and elastase-alpha(1)PI complex were determined using immunoluminometric assays. Elastase inhibition capacity (EIC) and elastase activity were determined using a colorimetric assay.
  
  
  RESULTS
  No EIC, but free elastase activity, was found in 82% of group 1, 20% of group 2, 20% of group 3 and 0% of group 4. Median MPO concentration was highest in group 1: 7,951 ng/ml (16th-84th percentile [16-84%]: 256-36,342) vs. 692 ng/ml (106-2,279; group 2), 332 ng/ml (98-1,657; group 3), and 0.12 ng/ml (0.08-0.26; group 4). Bronchiectasis patients with bronchial Pseudomonas infection showed higher amounts of neutrophils (p < 0.01) and higher elastase activity (p < 0.05) than patients with sterile lavage.
  
  
  CONCLUSIONS
  Bronchiectasis patients show a severe imbalance between neutrophil activity and protective molecules leading to possible lung destruction. Chronic Pseudomonas infection might trigger neutrophil activation. Future research and treatment strategies should focus on increased bacterial clearance and inhibition of neutrophil toxicity.
authors.affiliation: Division of Respiratory Diseases, Medical Clinic II, Medical University Lübeck, Germany. Bmschaaf@aol.com
authors.forename: B
authors.initials: B
authors.lastname: Schaaf
authors.forename: A
authors.initials: A
authors.lastname: Wieghorst
authors.forename: S P
authors.initials: SP
authors.lastname: Aries
authors.forename: K
authors.initials: K
authors.lastname: Dalhoff
authors.forename: J
authors.initials: J
authors.lastname: Braun
mesh_terms: D000328:Adult; D000368:Aged; D001987:Bronchiectasis / Q000276:immunology / Q000378:metabolism / Q000382:microbiology / Q000503:physiopathology*; D001992:Bronchoalveolar Lavage Fluid; D003124:Colorimetry; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D019272:Leukocyte Elastase / Q000032:analysis; D008297:Male; D008875:Middle Aged; D018375:Neutrophil Activation; D009195:Peroxidase / Q000032:analysis; D011014:Pneumonia / Q000276:immunology / Q000503:physiopathology*; D011658:Pulmonary Fibrosis / Q000276:immunology / Q000503:physiopathology*; D000515:alpha 1-Antitrypsin / Q000032:analysis
chemical_list: D000515:alpha 1-Antitrypsin; D009195:Peroxidase; D019272:Leukocyte Elastase