Noah T L, Wortman I A, Becker S
Center for Environmental Medicine and Lung Biology, The University of North Carolina at Chapel Hill 27599-7220, USA.
Immunopharmacology. 1998 Jun;39(3):193-9. doi: 10.1016/s0162-3109(98)00017-4.
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.
呼吸道合胞病毒（RSV）是婴儿细支气管炎的重要病因，是哮喘加重的重要诱因，并且在体外可刺激人呼吸道上皮细胞产生趋化因子。我们检测了皮质类固醇丙酸氟替卡松（FP）对人支气管上皮细胞系BEAS-2B受RSV刺激产生趋化因子白细胞介素8（IL-8）和调节激活正常T细胞表达和分泌因子（RANTES）的影响。将汇合的BEAS-2B培养物以约1个蚀斑形成单位/细胞接种RSV，并每隔24小时收集培养基。使用酶联免疫吸附测定法（ELISA）测量上清液中IL-8和RANTES的浓度。确定了不同浓度的FP对RSV诱导的趋化因子释放的影响。RSV刺激了IL-8和RANTES的释放增加，尤其是在病毒接种后24 - 48小时。当培养物用≥10^(-8) M（对于IL-8）或≥10^(-7) M（对于RANTES）的FP处理时，发现对两种趋化因子的RSV刺激增加有显著但不完全的抑制作用。FP对感染的BEAS-2B细胞释放RSV本身没有显著影响。我们得出结论，吸入性皮质类固醇在降低哮喘加重频率或严重程度方面发挥作用的一种可能机制是抑制气道细胞中病毒诱导的趋化因子产生。
