title: Biological markers in induced sputum of patients with different phenotypes of chronic airway obstruction.
abstract: BACKGROUND
  Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease characterized by a combination of 3 different disorders, namely chronic asthma, chronic bronchitis and pulmonary emphysema, sometimes simultaneously present in the same subject.
  
  
  OBJECTIVE
  The aim of our study was to compare sputum inflammatory markers in patients with different phenotypes of chronic airway obstruction.
  
  
  METHODS
  Forty-five subjects (forced expiratory volume in 1 s/vital capacity, FEV(1)/VC: 58.8 +/- 12.2%; FEV(1): 49.8 +/- 11.5% of predicted) were classified as chronic asthma (n = 10) or COPD patients (n = 35); the latter were further divided into patients with prevalent chronic bronchitis (n = 24) or prevalent pulmonary emphysema (n = 11) according to clinical history and functional evaluation, and underwent sputum induction and analysis of inflammatory cell and soluble mediators.
  
  
  RESULTS
  Patients with chronic asthma showed higher sputum eosinophil percentages and eosinophilic cationic protein levels, and lower neutrophil percentages and neutrophil elastase levels than COPD patients. Neutrophil chemotactic activity in sputum supernatant was higher than the pool of normal subjects both in chronic asthma and COPD patients. No difference in sputum cell composition and levels of soluble mediators was observed between patients with chronic bronchitis and patients with pulmonary emphysema.
  
  
  CONCLUSIONS
  The pattern of airway inflammation in induced sputum of patients with chronic asthma is different from that of COPD patients with a similar FEV(1). Among COPD patients, however, the pattern of airway inflammation shows no difference between chronic bronchitis and patients with pulmonary emphysema, suggesting that these two clinically and functionally distinct phenotypes share a common inflammatory pattern as detected by induced sputum.
authors.affiliation: Cardiothoracic and Vascular Department, University of Pisa, Pisa, Italy.
authors.forename: Maria Laura
authors.initials: ML
authors.lastname: Bartoli
authors.forename: Antonella
authors.initials: A
authors.lastname: Di Franco
authors.forename: Barbara
authors.initials: B
authors.lastname: Vagaggini
authors.forename: Elena
authors.initials: E
authors.lastname: Bacci
authors.forename: Silvana
authors.initials: S
authors.lastname: Cianchetti
authors.forename: Federico Lorenzo
authors.initials: FL
authors.lastname: Dente
authors.forename: Monica
authors.initials: M
authors.lastname: Tonelli
authors.forename: Pier Luigi
authors.initials: PL
authors.lastname: Paggiaro
mesh_terms: D000368:Aged; D001249:Asthma / Q000175:diagnosis* / Q000276:immunology / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism*; D029481:Bronchitis, Chronic / Q000175:diagnosis* / Q000276:immunology / Q000378:metabolism; D047150:Eosinophil Cationic Protein / Q000378:metabolism; D005260:Female; D006098:Granulocytes / Q000166:cytology; D006801:Humans; D016209:Interleukin-8 / Q000378:metabolism; D019272:Leukocyte Elastase / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D011656:Pulmonary Emphysema / Q000175:diagnosis* / Q000276:immunology / Q000378:metabolism; D013183:Sputum / Q000166:cytology / Q000276:immunology / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D016209:Interleukin-8; D047150:Eosinophil Cationic Protein; D019272:Leukocyte Elastase