title: Vascular remodeling is a feature of asthma and nonasthmatic eosinophilic bronchitis.
abstract: BACKGROUND
  Increased vascularity and expression of vascular endothelial growth factor (VEGF) are recognized features of the asthmatic airway. The association of vascular remodeling with airway hyperresponsiveness (AHR) is unclear.
  
  
  OBJECTIVE
  To assess vascular remodeling and sputum VEGF concentration in subjects with asthma, subjects with nonasthmatic eosinophilic bronchitis (EB), and healthy controls.
  
  
  METHODS
  In cohort 1, 19 patients with asthma (Global Initiative for Asthma [GINA] 1-2, n = 9; GINA 3-5, n = 10), 10 patients with EB, and 11 healthy matched controls were recruited. Expression of the endothelial marker EN4 was assessed in bronchial biopsy samples. Vessels were counted using the validated mean Chalkley count by a blind observer. For cohort 2, a second independent cohort of 31 patients with asthma (GINA 1-2, n = 11; GINA 3-5, n = 20), 14 patients with EB, and 15 matched controls was recruited. Induced sputum supernatant VEGF was measured by ELISA.
  
  
  RESULTS
  The mean chalkley count was significantly greater in GINA 3-5 asthma (5.2 [0.4]) and EB (4.8 [0.3]) compared with controls (3.5 [0.5]) and demonstrated a significant inverse correlation with the postbronchodilator FEV(1)% predicted in patients with asthma (R(2) = 0.28; P = .02). Sputum VEGF concentration was also increased in GINA 3-5 asthma (2365 [1361-4110] pg/g) and EB (4699 [2818-7834] pg/g) compared with controls (1094 [676-1774] pg/g) and was inversely related to postbronchodilator FEV(1)% predicted in asthma (R(2) = 0.2; P = .01).
  
  
  CONCLUSIONS
  Vascular remodeling is a feature of asthma, and EB and is inversely associated with the postbronchodilator FEV(1) in asthma, suggesting that vascular remodeling is associated with airflow obstruction but not AHR.
  
  
  CONCLUSIONS
  Vascular remodeling is dissociated from AHR in asthma and associated with airflow limitation.
authors.affiliation: Institute of Lung Health, University of Leicester, Leicester, United Kingdom.
authors.forename: Salman
authors.initials: S
authors.lastname: Siddiqui
authors.forename: Amanda
authors.initials: A
authors.lastname: Sutcliffe
authors.forename: Aarti
authors.initials: A
authors.lastname: Shikotra
authors.forename: Lucy
authors.initials: L
authors.lastname: Woodman
authors.forename: Camille
authors.initials: C
authors.lastname: Doe
authors.forename: Sue
authors.initials: S
authors.lastname: McKenna
authors.forename: Andrew
authors.initials: A
authors.lastname: Wardlaw
authors.forename: Peter
authors.initials: P
authors.lastname: Bradding
authors.forename: Ian
authors.initials: I
authors.lastname: Pavord
authors.forename: Christopher
authors.initials: C
authors.lastname: Brightling
mesh_terms: D000328:Adult; D001249:Asthma / Q000473:pathology* / Q000503:physiopathology; D001808:Blood Vessels / Q000473:pathology; D001980:Bronchi / Q000098:blood supply*; D016535:Bronchial Hyperreactivity / Q000209:etiology; D001991:Bronchitis / Q000473:pathology* / Q000503:physiopathology; D004802:Eosinophilia / Q000473:pathology* / Q000503:physiopathology; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D008297:Male; D008875:Middle Aged; D013183:Sputum / Q000737:chemistry; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis
chemical_list: D042461:Vascular Endothelial Growth Factor A