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Dual oxidase 2 is essential for the toll-like receptor 5-mediated inflammatory response in airway mucosa

DC Field Value Language
dc.contributor.author김창훈-
dc.contributor.author유지환-
dc.contributor.author윤주헌-
dc.contributor.author이상남-
dc.contributor.author주정희-
dc.date.accessioned2014-12-19T16:27:59Z-
dc.date.available2014-12-19T16:27:59Z-
dc.date.issued2012-
dc.identifier.issn1523-0864-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/89580-
dc.description.abstractAIMS: Airway mucosa is constantly exposed to various airborne microbes, and epithelial host defense requires a robust innate immunity. Recently, it has been suggested that NADPH oxidase (NOX) isozymes serve functional roles in toll-like receptor (TLR)-mediated innate immune responses. However, the molecular mechanism between TLR and NOX-mediated reactive oxygen species (ROS) production in human airway mucosa has been poorly understood. RESULTS: Here, we show that flagellin-induced ROS generation is dependent on dual oxidase 2 (DUOX2) activation, which is regulated by [Ca(2+)](i) mobilization in primary normal human nasal epithelial (NHNE) cells. Interestingly, we observed that silencing of DUOX2 expression in NHNE cells and nasal epithelium of Duox2 knockout mice failed to trigger mucin and MIP-2? production upon challenging flagellin. INNOVATION: Our observation in this study reveals that flagellin-induced hydrogen peroxide (H(2)O(2)) generation is critical for TLR5-dependent innate immune responses, including IL-8 production and MUC5AC expression in the nasal epithelium. Furthermore, DUOX2-mediated H(2)O(2) generation activated by the flagellin-TLR5 axis might serve as a novel therapeutic target for infectious inflammation diseases in the airway tract. CONCLUSION: Taken together, we propose that DUOX2 plays pivotal roles in TLR5-dependent inflammatory response of nasal airway epithelium.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfANTIOXIDANTS & REDOX SIGNALING-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHCalcium/metabolism-
dc.subject.MESHCluster Analysis-
dc.subject.MESHCytosol/metabolism-
dc.subject.MESHDual Oxidases-
dc.subject.MESHEpithelial Cells/metabolism-
dc.subject.MESHFlagellin/metabolism-
dc.subject.MESHGene Expression Profiling-
dc.subject.MESHGene Expression Regulation-
dc.subject.MESHHumans-
dc.subject.MESHInflammation/immunology-
dc.subject.MESHInflammation/metabolism*-
dc.subject.MESHInterleukin-8/immunology-
dc.subject.MESHInterleukin-8/metabolism-
dc.subject.MESHMice-
dc.subject.MESHMice, 129 Strain-
dc.subject.MESHMice, Inbred C57BL-
dc.subject.MESHMice, Knockout-
dc.subject.MESHMucin 5AC/immunology-
dc.subject.MESHMucin 5AC/metabolism-
dc.subject.MESHMutation-
dc.subject.MESHNADPH Oxidases/genetics-
dc.subject.MESHNADPH Oxidases/metabolism*-
dc.subject.MESHNasal Lavage Fluid/immunology-
dc.subject.MESHNeutrophil Infiltration/immunology-
dc.subject.MESHReactive Oxygen Species/metabolism-
dc.subject.MESHRespiratory Mucosa/immunology-
dc.subject.MESHRespiratory Mucosa/metabolism*-
dc.subject.MESHToll-Like Receptor 5/immunology-
dc.subject.MESHToll-Like Receptor 5/metabolism*-
dc.titleDual oxidase 2 is essential for the toll-like receptor 5-mediated inflammatory response in airway mucosa-
dc.typeArticle-
dc.contributor.collegeResearcher Institutes (부설 연구소)-
dc.contributor.department생체방어연구센터-
dc.contributor.googleauthorJung-Hee Joo-
dc.contributor.googleauthorJi-Hwan Ryu-
dc.contributor.googleauthorChang-Hoon Kim-
dc.contributor.googleauthorHyun Jik Kim-
dc.contributor.googleauthorMi-Sun Suh-
dc.contributor.googleauthorJin-Oh Kim-
dc.contributor.googleauthorSeung Yeun Chung-
dc.contributor.googleauthorSang Nam Lee-
dc.contributor.googleauthorHwan Mook Kim-
dc.contributor.googleauthorYun Soo Bae-
dc.contributor.googleauthorJoo-Heon Yoon-
dc.identifier.doi10.1196/annals.1378.032-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02604-
dc.contributor.localIdA02813-
dc.contributor.localIdA03958-
dc.contributor.localIdA01050-
dc.contributor.localIdA02522-
dc.relation.journalcodeJ00190-
dc.identifier.eissn1557-7716-
dc.identifier.pmid21714724-
dc.identifier.urlhttp://online.liebertpub.com/doi/abs/10.1089/ars.2011.3898-
dc.subject.keywordAnimals-
dc.subject.keywordCalcium/metabolism-
dc.subject.keywordCluster Analysis-
dc.subject.keywordCytosol/metabolism-
dc.subject.keywordDual Oxidases-
dc.subject.keywordEpithelial Cells/metabolism-
dc.subject.keywordFlagellin/metabolism-
dc.subject.keywordGene Expression Profiling-
dc.subject.keywordGene Expression Regulation-
dc.subject.keywordHumans-
dc.subject.keywordInflammation/immunology-
dc.subject.keywordInflammation/metabolism*-
dc.subject.keywordInterleukin-8/immunology-
dc.subject.keywordInterleukin-8/metabolism-
dc.subject.keywordMice-
dc.subject.keywordMice, 129 Strain-
dc.subject.keywordMice, Inbred C57BL-
dc.subject.keywordMice, Knockout-
dc.subject.keywordMucin 5AC/immunology-
dc.subject.keywordMucin 5AC/metabolism-
dc.subject.keywordMutation-
dc.subject.keywordNADPH Oxidases/genetics-
dc.subject.keywordNADPH Oxidases/metabolism*-
dc.subject.keywordNasal Lavage Fluid/immunology-
dc.subject.keywordNeutrophil Infiltration/immunology-
dc.subject.keywordReactive Oxygen Species/metabolism-
dc.subject.keywordRespiratory Mucosa/immunology-
dc.subject.keywordRespiratory Mucosa/metabolism*-
dc.subject.keywordToll-Like Receptor 5/immunology-
dc.subject.keywordToll-Like Receptor 5/metabolism*-
dc.contributor.alternativeNameKim, Chang Hoon-
dc.contributor.alternativeNameRyu, Ji Hwan-
dc.contributor.alternativeNameYoon, Joo Heon-
dc.contributor.alternativeNameLee, Sang Nam-
dc.contributor.alternativeNameJoo, Jung Hee-
dc.contributor.affiliatedAuthorYoon, Joo Heon-
dc.contributor.affiliatedAuthorLee, Sang Nam-
dc.contributor.affiliatedAuthorJoo, Jung Hee-
dc.contributor.affiliatedAuthorKim, Chang Hoon-
dc.contributor.affiliatedAuthorRyu, Ji Hwan-
dc.citation.volume16-
dc.citation.number1-
dc.citation.startPage57-
dc.citation.endPage70-
dc.identifier.bibliographicCitationANTIOXIDANTS & REDOX SIGNALING, Vol.16(1) : 57-70, 2012-
dc.identifier.rimsid32328-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Research Institute (부설연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Otorhinolaryngology (이비인후과학교실) > 1. Journal Papers

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