ISSN:
1398-9995
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
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-4Rα). 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 μg 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-4Rα immunoreactivity (rs = 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.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1398-9995.2005.00694.x
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