title: Effect of HFA-flunisolide on peripheral lung inflammation in asthma.
abstract: BACKGROUND
  New hydrofluoroalkane (HFA) formulations of glucocorticoids have been shown to effectively control asthma. HFA glucocorticoids are deposited across all sizes of airways, including the small ones. However, it is not clear whether they can suppress peripheral airway inflammation.
  
  
  OBJECTIVE
  We sought to determine whether HFA-flunisolide could suppress peripheral inflammation in asthma.
  
  
  METHODS
  Twelve patients with mild to moderate asthma received HFA-flunisolide for 6 weeks. Transbronchial and endobronchial biopsy specimens were obtained before and after treatment, and spirometry was performed. Changes in inflammatory cells (eosinophils, neutrophils, lymphocytes, macrophages, basophils) and IL-5 and eotaxin were measured by using immunocytochemistry and in situ hybridization.
  
  
  RESULTS
  Lung function significantly improved after treatment (P <.05). HFA-flunisolide significantly reduced eosinophils, IL-5, and eotaxin in both peripheral and central airways (P <.01). Neutrophils significantly increased after treatment in peripheral and central airways (P <.05). The numbers of lymphocytes remained unchanged.
  
  
  CONCLUSIONS
  These results show that HFA-flunisolide effectively suppressed eosinophilic inflammation in peripheral and central airways. These changes were accompanied by improvement in lung function.
authors.affiliation: Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada.
authors.forename: Hans-Peter
authors.initials: HP
authors.lastname: Hauber
authors.forename: Mark
authors.initials: M
authors.lastname: Gotfried
authors.forename: Kenneth
authors.initials: K
authors.lastname: Newman
authors.forename: Rahul
authors.initials: R
authors.lastname: Danda
authors.forename: Ronald J
authors.initials: RJ
authors.lastname: Servi
authors.forename: Pota
authors.initials: P
authors.lastname: Christodoulopoulos
authors.forename: Qutayba
authors.initials: Q
authors.lastname: Hamid
mesh_terms: D000328:Adult; D018927:Anti-Asthmatic Agents / Q000008:administration & dosage*; D001249:Asthma / Q000188:drug therapy* / Q000503:physiopathology; D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000235:genetics; D004804:Eosinophils / Q000187:drug effects*; D005260:Female; D005446:Fluocinolone Acetonide / Q000008:administration & dosage* / Q000031:analogs & derivatives*; D006801:Humans; D006845:Hydrocarbons, Fluorinated / Q000008:administration & dosage*; D007249:Inflammation / Q000188:drug therapy*; D015848:Interleukin-5 / Q000235:genetics; D008168:Lung / Q000187:drug effects* / Q000503:physiopathology; D008297:Male; D012333:RNA, Messenger / Q000032:analysis
chemical_list: D018927:Anti-Asthmatic Agents; C515456:CCL11 protein, human; D054413:Chemokine CCL11; D019742:Chemokines, CC; D006845:Hydrocarbons, Fluorinated; D015848:Interleukin-5; D012333:RNA, Messenger; D005446:Fluocinolone Acetonide; C007734:flunisolide