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Trichomonas vaginalis-induced neutrophil apoptosis causes anti-inflammatory cytokine production by human monocyte-derived macrophages

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dc.contributor.authorAhn, Myoung Hee-
dc.contributor.authorSong, Hyun-Ouk-
dc.contributor.authorRyu, Jae Sook-
dc.date.accessioned2022-12-21T01:44:34Z-
dc.date.available2022-12-21T01:44:34Z-
dc.date.issued2008-08-
dc.identifier.issn0141-9838-
dc.identifier.issn1365-3024-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/178071-
dc.description.abstractNeutrophils are the predominant inflammatory cells found in the vaginal discharge of patients with a Trichomonas vaginalis infection. Neutrophils have a shorter life span than other leucocytes. Our previous study indicated that live T. vaginalis alters Mcl-1 expression and caspase-3 activation, thereby inducing apoptosis of human neutrophils. However, it was previously unknown that the apoptotic neutrophils brought about by T. vaginalis can influence vaginal inflammation. Thus, human monocyte-derived macrophages (HMDM) were incubated with T. vaginalis-induced apoptotic neutrophils. Cytokine production and phagocytosis by HMDM were evaluated by ELISA and myeloperoxidase stain, respectively. HMDM showed increased anti-inflammatory cytokine production (IL-10) and decreased levels of pro-inflammatory cytokines, such as TNF-alpha and IL-6, compared with macrophages alone. Therefore, these results suggest that apoptotic neutrophils caused by T. vaginalis may lead to the resolution of vaginal inflammation by anti-inflammatory cytokine production in the human macrophages.-
dc.format.extent7-
dc.language영어-
dc.language.isoENG-
dc.publisherBlackwell Publishing Inc.-
dc.titleTrichomonas vaginalis-induced neutrophil apoptosis causes anti-inflammatory cytokine production by human monocyte-derived macrophages-
dc.typeArticle-
dc.publisher.location미국-
dc.identifier.doi10.1111/j.1365-3024.2008.01037.x-
dc.identifier.scopusid2-s2.0-64549160267-
dc.identifier.wosid000257701200004-
dc.identifier.bibliographicCitationParasite Immunology, v.30, no.8, pp 410 - 416-
dc.citation.titleParasite Immunology-
dc.citation.volume30-
dc.citation.number8-
dc.citation.startPage410-
dc.citation.endPage416-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaImmunology-
dc.relation.journalResearchAreaParasitology-
dc.relation.journalWebOfScienceCategoryImmunology-
dc.relation.journalWebOfScienceCategoryParasitology-
dc.subject.keywordPlusPHOSPHATIDYLSERINE RECEPTOR-
dc.subject.keywordPlusALVEOLAR MACROPHAGES-
dc.subject.keywordPlusACTIVATING CASPASE-3-
dc.subject.keywordPlusPROMOTES APOPTOSIS-
dc.subject.keywordPlusEPITHELIAL-CELLS-
dc.subject.keywordPlusPHAGOCYTOSIS-
dc.subject.keywordPlusINFLAMMATION-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusLEUKOCYTES-
dc.subject.keywordPlusRESOLUTION-
dc.subject.keywordAuthoranti-inflammatory cytokine-
dc.subject.keywordAuthorapoptotic neutrophil-
dc.subject.keywordAuthormacrophage-
dc.subject.keywordAuthorphagocytosis-
dc.subject.keywordAuthorTrichomonas vaginalis-
dc.identifier.urlhttps://onlinelibrary.wiley.com/doi/10.1111/j.1365-3024.2008.01037.x-
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