목적: We already reported that the regulated production of reactive oxygen species (ROS) by Duox2 and mitochondria has been considered a unique property of innate immune defense system. However, the alternative roles of both enzymes in nasal epithelium still need to be completely defined. We are especially interested in the differentiated antiviral activity of mitochondrial ROS against influenza A virus (IAV) infection in nasal epithelium and whether it might be influenced by IFN secretion after viral infection or not. 방법:We established a system for isolating (with endonasal brushing) and culturing (with air-liquid interface) human nasal epithelial cells (NEC) from normal volunteers. We used this system to assess the antiviral activity of mitochondrial ROS and relation with IFN signaling 결과:We observed that intracellular ROS generation was increased after 1 hr and 1 day post of infection (PI) in NEC and mitochondrial ROS was generated dominantly at 1 days after infection. IAV titer and mRNA levels were significantly higher in case of scavenging mitochondrial ROS. Both STAT1 and STAT2 phosphorylation and the mRNA levels of IFN-stimulated genes, including Mx1, 2,5-OAS1, IFIT1, and CXCL10, were induced after IAV infection up to PI 3 days. After suppression of mitochondrial ROS generation, IAV-induced phosphorylation of STAT and mRNA levels of IFN-stimulated genes were attenuated and actually, viral titers of IAV were significantly higher in cases with scavenging mitochondrial ROS. IAV-induced mitochondrial ROS generation was attenuated when secreted IFN-lambda was neutralized and if cells were transfected with shRNA of IFN-lambda binding receptors resulting in increase of IAV mRNA level and viral titer more significantly. 결론:Our findings suggest that mitochondrial ROS might be responsible for controlling IAV infection and may be potential sources of ROS generation, which is required to initiate an innate immune response through IFN-lambda in nasal epithelium.