title: Airway mast cells and eosinophils correlate with clinical severity and airway hyperresponsiveness in corticosteroid-treated asthma.
abstract: BACKGROUND
  The relationship between airway inflammation and asthma severity in corticosteroid-treated asthma is unclear.
  
  
  OBJECTIVE
  Our purpose was to characterize the inflammatory cell profile of the airway lumen and epithelium in corticosteroid-treated asthma and to relate these findings to clinical and physiologic markers of asthma severity.
  
  
  METHODS
  Adults (n = 20) with asthma received standardized high-dose inhaled corticosteroid therapy with beclomethasone 2000 microgram per day for 8 weeks. Airway responsiveness to methacholine and hypertonic (4.5%) saline solution was then assessed, followed by sputum induction and, 1 week later, bronchoscopy with bronchoalveolar lavage and bronchial brush biopsy to assess inflammatory cells.
  
  
  RESULTS
  Clinical asthma severity was associated with airway hyperresponsiveness. Metachromatic cells were the main granulocyte present in bronchial brush biopsy specimens and correlated with airway responsiveness to saline solution (r = -0.75), methacholine (r = -0.74), peak flow variability (r = 0.59), and clinical asthma severity (r = 0.57). Eosinophils were the main granulocyte present in sputum and correlated with airway responsiveness to saline solution (r = -0.63) but not with other clinical markers of asthma severity. Bronchoalveolar lavage cell counts were not related to clinical asthma severity.
  
  
  CONCLUSIONS
  In asthmatic patients treated with cortico-steroids, the dominant inflammatory effector cell in the epithelium is the metachromatic cell, and in sputum it is the eosinophil. These cells correlate with the degree of airway hyperresponsiveness. Clinical asthma severity correlates with airway responsiveness and epithelial metachromatic cells. Induced sputum eosinophils and airway responsiveness to hypertonic saline solution may be useful markers of airway inflammation for clinical practice.
authors.affiliation: Airways Research Centre, Department of Respiratory Medicine, John Hunter Hospital, Newcastle, Australia.
authors.forename: P G
authors.initials: PG
authors.lastname: Gibson
authors.forename: N
authors.initials: N
authors.lastname: Saltos
authors.forename: T
authors.initials: T
authors.lastname: Borgas
mesh_terms: D000328:Adult; D001249:Asthma / Q000188:drug therapy* / Q000503:physiopathology*; D001507:Beclomethasone / Q000627:therapeutic use*; D001980:Bronchi / Q000166:cytology*; D016535:Bronchial Hyperreactivity / Q000097:blood; D001991:Bronchitis / Q000473:pathology / Q000503:physiopathology; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D004305:Dose-Response Relationship, Drug; D004804:Eosinophils / Q000166:cytology*; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D008407:Mast Cells / Q000276:immunology*; D010366:Peak Expiratory Flow Rate / Q000187:drug effects; D012720:Severity of Illness Index
chemical_list: D005938:Glucocorticoids; D001507:Beclomethasone