title: Inflammatory biomarkers in airways of patients with severe asthma compared with non-severe asthma.
abstract: BACKGROUND
  About 5-10% of patients with asthma suffer from poorly-controlled disease despite corticosteroid (CS) therapy.
  
  
  OBJECTIVE
  We determined whether there were any differences in inflammatory biomarkers between severe and non-severe asthma patients.
  
  
  METHODS
  Nineteen severe and 20 non-severe asthma patients were recruited and underwent collection of induced sputum, bronchoalveolar lavage (BAL) fluid and bronchial biopsies.
  
  
  RESULTS
  Biopsy results showed no differences in eosinophils (major basic protein positive), neutrophils, macrophages, T cells and mast cells in the bronchial submucosa. However, subbasement membrane (SBM) thickness and smooth muscle area were increased in the biopsies. No significant differences were observed in the induced sputum inflammatory cells. In BAL fluid, there was a significant increase in neutrophils but a significant decrease in macrophages. Eosinophil counts were non-significantly increased threefold in both sputum and BAL in severe asthma. Levels of IL-8 and IL-13 in sputum supernatants were similar in both groups of asthma patients. There was a significant inverse correlation between post-bronchodilator forced expiratory volume in 1 s and provocative concentration of methacholine causing a 20% fall in FEV(1) with SBM thickness.
  
  
  CONCLUSIONS
  Differences in inflammatory cells were observed mainly in terms of increased neutrophils and reduction in macrophage numbers in BAL fluid with a trend towards increased eosinophils in severe asthma compared with non-severe asthma. However, the most notable features are the increase in features of airway wall remodelling of SBM thickness and smooth muscle area.
authors.affiliation: Experimental Studies, Airway Disease Section, National Heart and Lung Institute, Imperial College, London, UK.
authors.forename: P
authors.initials: P
authors.lastname: Macedo
authors.forename: M
authors.initials: M
authors.lastname: Hew
authors.forename: A
authors.initials: A
authors.lastname: Torrego
authors.forename: S
authors.initials: S
authors.lastname: Jouneau
authors.forename: T
authors.initials: T
authors.lastname: Oates
authors.forename: A
authors.initials: A
authors.lastname: Durham
authors.forename: K F
authors.initials: KF
authors.lastname: Chung
mesh_terms: D000328:Adult; D001249:Asthma / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D015415:Biomarkers / Q000378:metabolism; D005260:Female; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism*; D018793:Interleukin-13 / Q000378:metabolism*; D016209:Interleukin-8 / Q000378:metabolism*; D007962:Leukocytes / Q000378:metabolism* / Q000473:pathology; D008297:Male; D020545:Respiratory Mucosa / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D012720:Severity of Illness Index; D013183:Sputum / Q000378:metabolism
chemical_list: D015415:Biomarkers; C508606:CXCL8 protein, human; D018836:Inflammation Mediators; D018793:Interleukin-13; D016209:Interleukin-8