The disruption mechanism of innate immune system in RSV infected epithelial cells and search of its restoration compound.

呼吸道合胞病毒(RSV)是儿童呼吸道疾病最常见的病因之一。鼻上皮细胞(NEC)是呼吸道合胞病毒(RSV)的第一个暴露部位。NEC通过RSV感染诱生III型干扰素，而不仅仅是I型干扰素。我们的结果表明，病毒传感器之一的RIG-I对III型干扰素的产生起到了作用。抗菌剂磷霉素通过抑制转录因子NF-κB的活性，抑制呼吸道合胞病毒诱导的促炎性趋化因子RANTES的产生和肺炎链球菌受体血小板活化因子受体的表达。

Respiratory syncytial virus (RSV) is one of the most common causes of respiratory diseases in children. Nasal epithelial cell (NEC) is the first site exposure to RSV. NEC induced type-III IFN by RSV infection, but not merely type-I IFN. Our results showed that RIG-I, one of the virus sensors, contributed to this type-III IFN production. Fosfomycin, anti-bacterial agent, suppressed the RSV-induced a proinflammatory chemokine, RANTES production, and a receptor for Streptococcus pneumoniae, platelet-activating factor receptor expression, by inhibition of transcription factor NF-κB activity.