The effect of corticosteroid on RANTES and IL-8 mRNA expression in human bronchial epithelial cell line infected with respiratory syncytial virus / 천식및알레르기

ABSTRACT

BACKGROUND: Besides being a structural barrier for infectious pathogens, bronchial epithelium also participates actively in the modulation of airway inflammatory reactions through the synthesis of a variety of proinflammatory mediators such as RANTES (regulated on activation, normal T cell expressed & secreted) and IL-8 (interleukin 8) which are important chemokines for chemotaxis of eosinophils and neutrophils and their activation. Respiratory syncytial virus (RSV) which is the most common cause of bronchiolitis in infants is an important trigger of asthma exacerbation and stimulates chemokine production by human airway epithelial cells in vitro. OBJECTIVES: The objectives of this study are to determine the effects of dexamethasone (DX) on RSV induced RANTES and IL-8 gene expression and their production by BEAS-2B cell, a human bronchial epithelial cell line. METHODS: Then, total RNA of RANTES was collected at 6, 12, 24 and 48 hour intervals after inoculation with RSV and total RNA of IL-8 was collected at 2, 4 and 6 hour intervals after inoculation with RSV. Gene expressions of RANTES and IL-8 were determined by RT-PCR semi- quantitatively from total RNA. DX at varying concentrations (10-9, 10-8, 10-7, 10-6M) on RSV (MOI=1, MOI=10) induced chemokine production. RESULTS: Gene expressions of RANTES and IL-8 were higher in RSV infected group compared to the non-infected group at each time and at each MOI. Gene expressions of RANTES and IL-8 were decreased in DX-treated RSV infected groups compared to the non-treated RSV infected group and this tendency was prominent in higher concentrations of DX. CONCLUSION: DX may modulate the inflammatory response of the airway in RSV induced bronchiolitis and asthma exacerbation through the inhibition of virus-induced chemokine production by bronchial epithelial cells. Bronchial epithelium also participates actively in the modulation of airway inflammatory reactions through the synthesis of proinflammatory mediators such as RANTES and IL-8.