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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.