Reactive Oxygen Species, Interferon and Antiviral Innate Immune Response in Nasal Mucosa.
10.3342/kjorl-hns.2015.58.11.739
- Author:
Seung No HONG
1
;
Hyun Jik KIM
Author Information
1. Department of Otorhinolaryngology, Seoul National University College of Medicine, Seoul, Korea. hyunjerry@snu.ac.kr
- Publication Type:Review
- Keywords:
Innate immunity;
Interferon;
Nasal mucosa;
Reactive oxygen species
- MeSH:
Allergens;
Critical Pathways;
Cytokines;
Humans;
Immunity, Innate*;
Influenza A virus;
Interferons*;
Nasal Mucosa*;
Phagocytes;
Reactive Oxygen Species*;
Respiratory Mucosa;
Respiratory System;
Transcription Factors
- From:Korean Journal of Otolaryngology - Head and Neck Surgery
2015;58(11):739-743
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
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.
