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dc.contributor.authorMoon, HGko
dc.contributor.authorKang, CSko
dc.contributor.authorChoi, JPko
dc.contributor.authorChoi, DSko
dc.contributor.authorChoi, HIko
dc.contributor.authorChoi, YWko
dc.contributor.authorJeon, SGko
dc.contributor.authorYoo, JYko
dc.contributor.authorJang, MHko
dc.contributor.authorGho, YSko
dc.contributor.authorKim, YKko
dc.date.available2016-03-31T08:26:48Z-
dc.date.created2013-03-04-
dc.date.issued2013-01-
dc.identifier.citationEXPERIMENTAL AND MOLECULAR MEDICINE, v.18, no.45, pp.E6-
dc.identifier.issn1226-3613-
dc.identifier.other2013-OAK-0000028106-
dc.identifier.urihttp://oasis.postech.ac.kr/handle/2014.oak/15323-
dc.description.abstractT-helper (Th) 17 cell responses are important for the development of neutrophilic inflammatory disease. Recently, we found that acetyl salicylic acid (ASA) inhibited Th17 airway inflammation in an asthma mouse model induced by sensitization with lipopolysaccharide (LPS)-containing allergens. To investigate the mechanism(s) of the inhibitory effect of ASA on the development of Th17 airway inflammation, a neutrophilic asthma mouse model was generated by intranasal sensitization with LPS plus ovalbumin (OVA) and then challenged with OVA alone. Immunologic parameters and airway inflammation were evaluated 6 and 48 h after the last OVA challenge. ASA inhibited the production of interleukin (IL)-17 from lung T cells as well as in vitro Th17 polarization induced by IL-6. Additionally, ASA, but not salicylic acid, suppressed Th17 airway inflammation, which was associated with decreased expression of acetyl-STAT3 (downstream signaling of IL-6) in the lung. Moreover, the production of IL-6 from inflammatory cells, induced by IL-17, was abolished by treatment with ASA, whereas that induced by LPS was not. Altogether, ASA, likely via its acetyl moiety, inhibits Th17 airway inflammation by blockade of IL-6 and IL-17 positive feedback. Experimental & Molecular Medicine (2013) 45, e5-
dc.description.abstractdoi:10.1038/emm.2013.10-
dc.description.abstractpublished online 18 January 2013-
dc.description.statementofresponsibilityX-
dc.languageEnglish-
dc.publisherSeoul : Korean Society of Medical Biochemistry and Molecular-
dc.subjectAcetyl salicylic acid-
dc.subjectIL-6-
dc.subjectIL-17A-
dc.subjectSTAT3-
dc.subjectTh17-
dc.subjectT-HELPER-CELLS-
dc.subjectPROSTAGLANDIN SYNTHESIS-
dc.subjectFAMILY CYTOKINES-
dc.subjectDENDRITIC CELLS-
dc.subjectKAPPA-B-
dc.subjectSTAT3-
dc.subjectDISEASE-
dc.subjectASPIRIN-
dc.subjectASTHMA-
dc.subjectINTERLEUKIN-17-
dc.titleAcetyl salicylic acid inhibits Th17 airway inflammation via blockade of IL-6 and IL-17 positive feedback.-
dc.typeArticle-
dc.contributor.college생명과학과-
dc.identifier.doi10.1038/EMM.2013.10-
dc.author.googleMoon, HG-
dc.author.googleKang, CS-
dc.author.googleChoi, JP-
dc.author.googleChoi, DS-
dc.author.googleChoi, HI-
dc.author.googleChoi, YW-
dc.author.googleJeon, SG-
dc.author.googleYoo, JY-
dc.author.googleJang, MH-
dc.author.googleGho, YS-
dc.author.googleKim, YK-
dc.relation.volume45-
dc.relation.startpageE5-
dc.contributor.id10138843-
dc.publisher.locationUK-
dc.relation.journalEXPERIMENTAL & MOLECULAR MEDICINE-
dc.relation.indexSCI급, SCOPUS 등재논문-
dc.relation.sciSCI-
dc.collections.nameJournal Papers-
dc.type.rimsART-
dc.contributor.localauthorGho, YS-
dc.contributor.localauthorKim, YK-
dc.contributor.nonIdAuthorMoon, HG-
dc.contributor.nonIdAuthorKang, CS-
dc.contributor.nonIdAuthorChoi, JP-
dc.contributor.nonIdAuthorChoi, DS-
dc.contributor.nonIdAuthorChoi, HI-
dc.contributor.nonIdAuthorChoi, YW-
dc.contributor.nonIdAuthorJeon, SG-
dc.contributor.nonIdAuthorYoo, JY-
dc.contributor.nonIdAuthorJang, MH-
dc.identifier.wosid000316788600005-
dc.date.tcdate2019-01-01-
dc.citation.number45-
dc.citation.startPageE6-
dc.citation.titleEXPERIMENTAL AND MOLECULAR MEDICINE-
dc.citation.volume18-
dc.identifier.localId0000028106-
dc.identifier.localId0000031576-
dc.identifier.scopusid2-s2.0-84876197796-
dc.description.journalClass1-
dc.description.wostc7-
dc.description.scptc2*
dc.date.scptcdate2018-05-121*

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Dept of Life Sciences
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