title: Effect of inhaled corticosteroid on an immunoreactive thymus and activation-regulated chemokine expression in the bronchial biopsies from asthmatics.
abstract: BACKGROUND
  Bronchial asthma is characterized by airway inflammation, notably because of eosinophils and T cells. Thymus and activation-regulated chemokine (TARC) is known to selectively attract Th2 cells, and is increased in response to interleukin (IL)-4 and IL-13, which share a common receptor, IL-4 receptor alpha (IL-4Ralpha). While corticosteroids have proven, very effective in modifying airway inflammation, the effect of corticosteroids on TARC in asthmatics has been little studied.
  
  
  OBJECTIVE
  We examined the effects of inhaled budesonide (BUD) on the expression of TARC and the number of inflammatory cells in bronchial biopsy specimens taken from asthma patients.
  
  
  METHODS
  Inhaled BUD 800 mug daily, or placebo was administered for 3 months in a double-blind, parallel-group study, and bronchial biopsies were performed before and after treatment. Biopsy specimens were examined by immunocytochemistry.
  
  
  RESULTS
  We observed a significant decrease in the epithelial expression of TARC (P < 0.01) in the BUD group compared with the placebo group. This was accompanied by decreases in the number of eosinophils (P < 0.01), CD3(+) T cells (P < 0.05), and CD4(+) T cells (P < 0.01). A significant correlation was found between changes in epithelial TARC and in IL-4Ralpha immunoreactivity (r(s) = 0.66, P < 0.01).
  
  
  CONCLUSIONS
  These findings suggest that corticosteroid asthma treatment can reduce infiltration of the airway by inflammatory cells, an effect modulated by down-regulation of bronchial epithelial TARC expression.
authors.affiliation: Department of Internal Medicine, Division of Respiratory and Infectious Diseases, St Marianna School of Medicine, Kawasaki, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Hoshino
authors.forename: T
authors.initials: T
authors.lastname: Nakagawa
authors.forename: Y
authors.initials: Y
authors.lastname: Sano
authors.forename: K
authors.initials: K
authors.lastname: Hirai
mesh_terms: D000280:Administration, Inhalation; D000328:Adult; D001249:Asthma / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology; D001706:Biopsy; D001980:Bronchi / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D001993:Bronchodilator Agents / Q000008:administration & dosage* / Q000627:therapeutic use; D019819:Budesonide / Q000008:administration & dosage* / Q000627:therapeutic use; D017252:CD3 Complex / Q000378:metabolism; D018791:CD4 Lymphocyte Count; D054414:Chemokine CCL17; D019742:Chemokines, CC / Q000378:metabolism*; D004311:Double-Blind Method; D004804:Eosinophils / Q000473:pathology; D005260:Female; D006801:Humans; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D013601:T-Lymphocytes / Q000378:metabolism / Q000473:pathology
chemical_list: D001993:Bronchodilator Agents; C106230:CCL17 protein, human; D017252:CD3 Complex; D054414:Chemokine CCL17; D019742:Chemokines, CC; D019819:Budesonide