title: Characteristics of eosinophilic and non-eosinophilic asthma during treatment with inhaled corticosteroids.
abstract: OBJECTIVE
  Eosinophilic inflammation in the respiratory tract is a hallmark of bronchial asthma. In naïve cases, the inflammatory profile is associated with disease severity and reactivity to inhaled corticosteroids (ICS). Sustained airway eosinophilia has been reported during ICS treatment. However, the immunological characteristics of these cases are not known and it is unclear if this situation contributes to asthma control. This study was performed to determine the answer of these questions.
  
  
  METHODS
  To compare phenotypes of eosinophilic and non-eosinophilic asthma (EA and NEA, respectively) under ICS treatment, clinical data were obtained from asthmatic subjects (n = 22) and healthy controls (n = 10), and the leukocyte compositions of induced sputum and peripheral blood were determined. T lymphocyte profiles in systemic blood were assessed by flow cytometry.
  
  
  RESULTS
  A higher frequency of emergency room visits was observed in the NEA group, which had a higher neutrophil count relative to the total inflammatory cell population in induced sputum than the EA group (59.5 versus 36.6%; p < 0.01). The fraction of helper T (Th)17 lymphocytes as well as the ratio of Th17 to regulatory T cells (Treg) in the peripheral blood was higher in the NEA than in the EA group (0.24 versus 0.13; p < 0.05).
  
  
  CONCLUSIONS
  Th17 were more prevalent than Treg cells in the peripheral blood of NEA patients under ICS treatment, corresponding to neutrophil-dominant airway inflammation and a severe asthmatic phenotype. Thus, an imbalance in Th17/Treg may be associated with the pathogenesis of NEA in patients undergoing ICS treatment.
authors.affiliation: Division of Respiratory Medicine, Department of Homeostatic Regulation and Development, Graduate School of Medical and Dental Sciences, Niigata University , Niigata , Japan , and.
authors.forename: Toshiki
authors.initials: T
authors.lastname: Furukawa
authors.forename: Takuro
authors.initials: T
authors.lastname: Sakagami
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Koya
authors.forename: Takashi
authors.initials: T
authors.lastname: Hasegawa
authors.forename: Hidenori
authors.initials: H
authors.lastname: Kawakami
authors.forename: Yosuke
authors.initials: Y
authors.lastname: Kimura
authors.forename: Yoshifumi
authors.initials: Y
authors.lastname: Hoshino
authors.forename: Hirotaka
authors.initials: H
authors.lastname: Sakamoto
authors.forename: Kenjiro
authors.initials: K
authors.lastname: Shima
authors.forename: Keisuke
authors.initials: K
authors.lastname: Tsukioka
authors.forename: Mio
authors.initials: M
authors.lastname: Toyama
authors.forename: Masachika
authors.initials: M
authors.lastname: Hayashi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kagamu
authors.forename: Ei-Ichi
authors.initials: E
authors.lastname: Suzuki
authors.forename: Ichiei
authors.initials: I
authors.lastname: Narita
mesh_terms: D000280:Administration, Inhalation; D000305:Adrenal Cortex Hormones / Q000008:administration & dosage / Q000627:therapeutic use*; D001249:Asthma / Q000188:drug therapy* / Q000276:immunology*; D004636:Emergency Service, Hospital / Q000706:statistics & numerical data; D004802:Eosinophilia / Q000150:complications / Q000276:immunology*; D005541:Forced Expiratory Volume; D006801:Humans; D007962:Leukocytes / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology; D013183:Sputum / Q000166:cytology; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D000305:Adrenal Cortex Hormones
keywords: Eosinophilic asthma; Th17 cell; inhaled cortico-steroid; non-eosinophilic asthma; regulatory T cell