Article

The effect of fluticasone propionate on respiratory syncytial virus-induced chemokine release by a human bronchial epithelial cell line.

Center for Environmental Medicine and Lung Biology, The University of North Carolina at Chapel Hill 27599-7220, USA.
Immunopharmacology 07/1998; 39(3):193-9. DOI:10.1016/S0162-3109(98)00017-4 pp.193-9
Source: PubMed

ABSTRACT Respiratory syncytial virus (RSV) is an important cause of bronchiolitis in infants, is an important trigger of asthma exacerbation, and stimulates chemokine production by human respiratory epithelial cells in vitro. We tested the effect of the corticosteroid fluticasone propionate (FP) on RSV-stimulated production of the chemokines interleukin 8 (IL-8) and RANTES (regulated upon activation, normal T cell expressed and secreted) by a human bronchial epithelial cell line, BEAS-2B. Confluent BEAS-2B cultures were inoculated with RSV at approximately 1 plaque-forming unit/cell, and media were collected at 24 h intervals. Concentrations of IL-8 and RANTES were measured in supernatants using ELISA. The effect of FP at varying concentrations on RSV-induced chemokine release was determined. RSV stimulated increased release of both IL-8 and RANTES, particularly at 24-48 h after virus inoculation. Significant but incomplete inhibition of RSV-stimulated increases for both chemokines was found when cultures were treated with FP at > or = 10(-8) M (for IL-8) or > or = 10(-7) M (for RANTES). There was no significant effect of FP on release of RSV itself from infected BEAS-2B cells. We conclude that a possible mechanism for the efficacy of inhaled corticosteroids in reducing the frequency or severity of asthma exacerbations is inhibition of virus-induced chemokine production by airway cells.

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Keywords

1 plaque-forming unit/cell
 
24 h intervals
 
airway cells
 
asthma exacerbations
 
BEAS-2B cells
 
chemokines interleukin 8
 
Confluent BEAS-2B cultures
 
corticosteroid fluticasone propionate
 
human bronchial epithelial cell line
 
human respiratory epithelial cells
 
IL-8
 
incomplete inhibition
 
normal T cell
 
possible mechanism
 
Respiratory syncytial virus
 
RSV-induced chemokine release
 
RSV-stimulated production
 
significant effect
 
stimulates chemokine production
 
virus-induced chemokine production