Reactive Oxygen Species, Interferon and Antiviral Innate Immune Response in Nasal Mucosa

Abstract

Received June 3, 2015 Accepted July 31, 2015 Address for correspondence Hyun Jik Kim, MD, PhD Department of Otorhinolaryngology, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul 03080, Korea Tel +82-2-2072-2203 Fax +82-2-735-2387 E-mail hyunjerry@snu.ac.kr The regulated production of reactive oxygen species (ROS) has been considered a unique property of phagocytic cells which use this ROS system to induce innate defense system that enables it to successfully combat the pathogens. However, the mechanisms for how respiratory mucosa might produce ROS against respiratory viral infection still need to be completely defined. Respiratory mucosa and nasal epithelium has been known as the first defense site of human respiratory tract which is highly exposed and vulnerable to environmental pathogens, including air-bone microbes, viruses and allergens. We are especially interested in the innate immune response to respiratory virus infection in nasal epithelium and how this response might be influenced by ROS generation after viral infection. The interferon (IFN) signaling system is perhaps the most critical pathway for antiviral defense and protective actions of IFNs rely on signaling through IFN receptors, transcription factors and IFN-stimulated genes or antiviral cytokines requiring for virus degradation and suppression of viral transcription or translation. We verified that both type I and type III IFN genes expression and secreted proteins were more highly induced after influenza A virus infection in nasal epithelium. We also propose that type III IFNs are the primary IFNs to mediate an anti-viral defense in nasal epithelium and more sensitively reacted with ROS which were produced after respiratory virus infection. We estimate that ROS are necessary for the innate immune response and trigger the induction of IFN-related innate immune response to resist respiratory virus infection in human respiratory mucosa. Korean J Otorhinolaryngol-Head Neck Surg 2015;58(11):739-43