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Effect of inhaled corticosteroid on an immunoreactive thymus and activation‐regulated chemokine expression in the bronchial biopsies from asthmatics
Author(s) -
Hoshino M.,
Nakagawa T.,
Sano Y.,
Hirai K.
Publication year - 2005
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/j.1398-9995.2005.00694.x
Subject(s) - budesonide , chemokine , medicine , asthma , placebo , inflammation , immunology , eosinophil , cc chemokine receptors , infiltration (hvac) , immunocytochemistry , allergy , chemokine receptor , pathology , physics , alternative medicine , thermodynamics
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‐4R α ). 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 μ g 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‐4R α 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.