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

DC FieldValueLanguage
dc.contributor.author김수진-
dc.contributor.author김창훈-
dc.contributor.author윤주헌-
dc.contributor.author정효진-
dc.date.accessioned2018-03-26T17:09:31Z-
dc.date.available2018-03-26T17:09:31Z-
dc.date.issued2015-
dc.identifier.issn0166-3542-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/157254-
dc.description.abstractThe 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.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherElsevier-
dc.relation.isPartOfANTIVIRAL RESEARCH-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHCarrier Proteins/genetics-
dc.subject.MESHCells, Cultured-
dc.subject.MESHChemokine CXCL10/genetics-
dc.subject.MESHHumans-
dc.subject.MESHImmunity, Innate/genetics*-
dc.subject.MESHImmunity, Innate/immunology-
dc.subject.MESHInfluenza A Virus, H1N1 Subtype/immunology*-
dc.subject.MESHInfluenza A Virus, H1N1 Subtype/pathogenicity-
dc.subject.MESHInterferons/genetics-
dc.subject.MESHMitochondria/metabolism*-
dc.subject.MESHMyxovirus Resistance Proteins/genetics-
dc.subject.MESHNasal Mucosa/immunology*-
dc.subject.MESHNasal Mucosa/virology*-
dc.subject.MESHPhosphorylation-
dc.subject.MESHReactive Oxygen Species/metabolism*-
dc.subject.MESHSTAT1 Transcription Factor/genetics-
dc.subject.MESHSTAT2 Transcription Factor/genetics-
dc.subject.MESHViral Load-
dc.titleMitochondrial reactive oxygen species modulate innate immune response to influenza A virus in human nasal epithelium-
dc.typeArticle-
dc.contributor.collegeResearch Institutes-
dc.contributor.departmentResearch Center for Human Natural Defense System-
dc.contributor.googleauthorSujin Kim-
dc.contributor.googleauthorMin-Ji Kim-
dc.contributor.googleauthorDo Yang Park-
dc.contributor.googleauthorHyo Jin Chung-
dc.contributor.googleauthorChang-Hoon Kim-
dc.contributor.googleauthorJoo-Heon Yoon-
dc.contributor.googleauthorHyun Jik Kim-
dc.identifier.doi10.1016/j.antiviral.2015.04.011-
dc.contributor.localIdA05230-
dc.contributor.localIdA01050-
dc.contributor.localIdA02604-
dc.contributor.localIdA03791-
dc.relation.journalcodeJ02902-
dc.identifier.eissn1872-9096-
dc.identifier.pmid25930096-
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S0166354215001035-
dc.subject.keywordInfluenza A virus-
dc.subject.keywordInterferon-stimulated genes-
dc.subject.keywordMitochondria-
dc.subject.keywordReactive oxygen species-
dc.contributor.alternativeNameKim, Sujin-
dc.contributor.alternativeNameKim, Chang Hoon-
dc.contributor.alternativeNameYoon, Joo Heon-
dc.contributor.alternativeNameChung, Hyo Jin-
dc.contributor.affiliatedAuthorKim, Sujin-
dc.contributor.affiliatedAuthorKim, Chang Hoon-
dc.contributor.affiliatedAuthorYoon, Joo Heon-
dc.contributor.affiliatedAuthorChung, Hyo Jin-
dc.citation.volume119-
dc.citation.startPage78-
dc.citation.endPage83-
dc.identifier.bibliographicCitationANTIVIRAL RESEARCH, Vol.119 : 78-83, 2015-
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

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