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Mitochondrial reactive oxygen species modulate innate immune response to influenza A virus in human nasal epithelium

Authors
 Sujin Kim  ;  Min-Ji Kim  ;  Do Yang Park  ;  Hyo Jin Chung  ;  Chang-Hoon Kim  ;  Joo-Heon Yoon  ;  Hyun Jik Kim 
Citation
 ANTIVIRAL RESEARCH, Vol.119 : 78-83, 2015 
Journal Title
 ANTIVIRAL RESEARCH 
ISSN
 0166-3542 
Issue Date
2015
MeSH
Carrier Proteins/genetics ; Cells, Cultured ; Chemokine CXCL10/genetics ; Humans ; Immunity, Innate/genetics* ; Immunity, Innate/immunology ; Influenza A Virus, H1N1 Subtype/immunology* ; Influenza A Virus, H1N1 Subtype/pathogenicity ; Interferons/genetics ; Mitochondria/metabolism* ; Myxovirus Resistance Proteins/genetics ; Nasal Mucosa/immunology* ; Nasal Mucosa/virology* ; Phosphorylation ; Reactive Oxygen Species/metabolism* ; STAT1 Transcription Factor/genetics ; STAT2 Transcription Factor/genetics ; Viral Load
Keywords
Influenza A virus ; Interferon-stimulated genes ; Mitochondria ; Reactive oxygen species
Abstract
The innate immune system of the nasal epithelium serves as a first line of defense against invading respiratory viruses including influenza A virus (IAV). Recently, it was verified that interferon (IFN)-related immune responses play a critical role in local antiviral innate immunity. Reactive oxygen species (ROS) generation by exogenous pathogens has also been demonstrated in respiratory epithelial cells and modulation of ROS has been reported to be important for respiratory virus-induced innate immune mechanisms. Passage-2 normal human nasal epithelial (NHNE) cells were inoculated with IAV (WS/33, H1N1) to assess the sources of IAV-induced ROS and the relationship between ROS and IFN-related innate immune responses. 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 three days post infection. Similarly, we observed that mitochondrial ROS generation increased maximally at 2 days after IAV infection. 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 ROS. 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 in NHNE cells.
Full Text
https://www.sciencedirect.com/science/article/pii/S0166354215001035
DOI
10.1016/j.antiviral.2015.04.011
Appears in Collections:
5. Research Institutes (연구소) > Research Center for Human Natural Defense System (생체방어연구센터) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Otorhinolaryngology (이비인후과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Sujin(김수진)
Kim, Chang Hoon(김창훈) ORCID logo https://orcid.org/0000-0003-1238-6396
Yoon, Joo Heon(윤주헌)
Chung, Hyo Jin(정효진)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/157254
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