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dc.contributor.author조석현-
dc.date.accessioned2018-02-28T04:33:13Z-
dc.date.available2018-02-28T04:33:13Z-
dc.date.issued2012-09-
dc.identifier.citationPlos One, Apr 2012, 4(7)en_US
dc.identifier.issn1932-6203-
dc.identifier.urihttp://journals.plos.org/plosone/article?id=10.1371/journal.pone.0035114-
dc.description.abstractBackground: Eosinophilic inflammation is a hallmark of chronic rhinosinusitis with nasal polyps. To model this disease process experimentally, nasal sensitization of mice with ovalbumin or aspergillus has been described. Here, we describe a genetically mutant mouse that develops robust spontaneous nasal eosinophilic inflammation. These mice lack the enzyme SHP-1 that down-regulates the IL-4R alpha/stat6 signaling pathway. We compared nasal inflammation and inflammatory mediators in SHP-1 deficient mice (mev) and an ovalbumin-induced nasal allergy model.Methods: A novel technique of trans-pharyngeal nasal lavage was developed to obtain samples of inflammatory cells from the nasal passages of allergic and mev mice. Total and differential cell counts were performed on cytospin preparations. Expression of tissue mRNA for IL-4, IL-13, and mouse beta-defensin-1 (MBD-1) was determined by quantitative PCR. Eotaxin in the lavage fluid was assessed by ELISA.Results: Allergic and mev mice had increased total cells and eosinophils compared with controls. Expression of IL-4 was similarly increased in both allergic and mev mice, but expression of IL-13 and eotaxin was significantly greater in the allergic mice than mev mice. Eotaxin was significantly up-regulated in both allergic rhinitis and mev mice. In both models of eosinophilic inflammation, down-regulation of the innate immune marker MBD-1 was observed.Conclusions: The mev mice display spontaneous chronic nasal eosinophilic inflammation with potential utility for chronic rhinosinusitis with nasal polyps research. The eosinophilic infiltrate is more robust in the mev mice than allergic mice, but Th2 cytokine expression is not as pronounced. Decreased MBD-1 expression in both models supports the concept that Th2-cytokines down-regulate sinonasal innate immunity in humans, and suggests a role for mouse models in investigating the interaction between adaptive and innate immunity in the sinonasal mucosa.en_US
dc.description.sponsorshipFunding was provided by the National Institutes of Health, National Institute of Allergy and Infectious Disease AI072502 (A.P.L.), and National Heart, Lung, and Blood Institute HL079349 (Z.Z.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.en_US
dc.language.isoenen_US
dc.publisherPublic Library Scienceen_US
dc.subjectCHRONIC RHINOSINUSITISen_US
dc.subjectAIRWAY INFLAMMATIONen_US
dc.subjectIMMUNODEFICIENT MUTANTen_US
dc.subjectINNATE IMMUNITYen_US
dc.subjectMURINE MODELen_US
dc.subjectMOTH-EATENen_US
dc.subjectBACTERIALen_US
dc.subjectRHINITISen_US
dc.subjectPATHOLOGYen_US
dc.subjectRECEPTORen_US
dc.titleSpontaneous Eosinophilic Nasal Inflammation in a Genetically-Mutant Mouse: Comparative Study with an Allergic Inflammation Modelen_US
dc.typeArticleen_US
dc.relation.no4-
dc.relation.volume7-
dc.identifier.doi10.1371/journal.pone.0035114-
dc.relation.page1-7-
dc.relation.journalPLOS ONE-
dc.contributor.googleauthorCho, Seok Hyun-
dc.contributor.googleauthorOh, Sun Young-
dc.contributor.googleauthorZhou Zhu-
dc.contributor.googleauthorLee, Joan-
dc.contributor.googleauthorLane, Andrew P.-
dc.contributor.googleauthor조석현-
dc.contributor.googleauthor오선영-
dc.contributor.googleauthor이조안-
dc.relation.code2012219766-
dc.sector.campusS-
dc.sector.daehakCOLLEGE OF MEDICINE[S]-
dc.sector.departmentDEPARTMENT OF MEDICINE-
dc.identifier.pidshcho-


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