목적: Nasal epithelium has been known as the first defense organ against aggressive respiratory viral infection and interferon- related innate immune system including pathogen recognition receptors (PRR) system might be critical for controlling respiratory viruses. The regulated production of reactive oxygen species (ROS) has been considered a unique property of nasal epithelial cells which use this ROS system to induce innate defense system. Our goal of this study is to determine the function of IAV-induced ROS as innate immune defense system requiring for the activation of PRR in nasal epithelium. 방법:20 Mice (C57BL/6J, male, 7-10 week) were anesthetized and challenged by intranasal administration of 213 pfu/30 ul of IAV (WS/33/H1N1) and were euthanized either 3, 7, 10 and 14 days post of infection for collecting nasal mucosa and NAL fluid. 결과:We already found that Duox2 generated ROS rapidly after IAV infection in nasal epithelium and that knockdown of Duox2 aggravated IAV infection. In addition, Duox2-derived ROS enhancement significantly suppressed IAV infection in nasal epithelium. In particular, Duox2-derived ROS were required for the induction of RIG-I, and MDA5 transcription. Following intranasal IAV inoculation into mice, viral infection was significantly aggravated from 3 days post-infection (dpi) in the nasal mucosa and the IAV viral titer was highest at 7 dpi. Both RIG-I and MDA5 mRNA levels increased dominantly in mouse nasal mucosa from 3 dpi consistent with this, RIG-I and MDA5 proteins were also induced after IAV infection. Both RIG-I and MDA5 mRNA levels and protein expression were induced to a lower extent in the nasal mucosa of the mice which were inoculated Duox2 shRNA and the IAV viral titer was significantly higher in nasal lavage. 결론:Duox2-derived ROS may be crucial for the clearance of Influenza virus in nasal epithelium. The absence of Duox2 leads to dysregulation of RIG-I and MDA5 and impedes efficient innate immunity against IAV infection.