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Effects of gallic acid on signaling kinases in murine macrophages and immune modulation against Brucella abortus 544 infection in mice

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dc.contributor.authorReyes, Alisha Wehdnesday Bernardo-
dc.contributor.authorArayan, Lauren Togonon-
dc.contributor.authorHop, Huynh Tan-
dc.contributor.authorTran Xuan Ngoc Huy-
dc.contributor.authorVu, Son Hai-
dc.contributor.authorMin, WonGi-
dc.contributor.authorLee, Hu Jang-
dc.contributor.authorKim, Suk-
dc.date.accessioned2022-12-26T17:01:51Z-
dc.date.available2022-12-26T17:01:51Z-
dc.date.created2022-12-13-
dc.date.issued2018-06-
dc.identifier.issn0882-4010-
dc.identifier.urihttps://scholarworks.bwise.kr/gnu/handle/sw.gnu/11623-
dc.description.abstractIn this study, we investigated the effects of gallic acid (GA) in intracellular signaling within murine macrophages and its contribution to host immunity during Brucella infection. In vitro analysis revealed that GA treatment decreased F-actin content and suppressed p38 alpha phosphorylation level. In vivo analysis showed that GA treatment reduced inflammation and proliferation of Brucella in spleens of mice in comparison to PBS treatment yielding a significant protection unit. For the analysis of immune response, the uninfected GA-treated mice showed increased production of IFN-gamma and MCP-1, and the Brucella-infected GA-treated mice showed elevated levels of IL-12p70, TNF, IFN-gamma, MCP-1, IL-10 and IL-6 in comparison to negative and positive control groups, respectively. These findings demonstrate the therapeutic effects of GA against Brucella infection through interference on intracellular signaling pathway, induction of cytokine production and protection from bacterial proliferation in spleens of mice.-
dc.language영어-
dc.language.isoen-
dc.publisherACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD-
dc.subjectCYTOKINE PRODUCTION-
dc.subjectIN-VITRO-
dc.subjectPATHOGENESIS-
dc.subjectRELEASE-
dc.titleEffects of gallic acid on signaling kinases in murine macrophages and immune modulation against Brucella abortus 544 infection in mice-
dc.typeArticle-
dc.contributor.affiliatedAuthorMin, WonGi-
dc.contributor.affiliatedAuthorLee, Hu Jang-
dc.contributor.affiliatedAuthorKim, Suk-
dc.identifier.doi10.1016/j.micpath.2018.04.032-
dc.identifier.scopusid2-s2.0-85046133810-
dc.identifier.wosid000436385300036-
dc.identifier.bibliographicCitationMICROBIAL PATHOGENESIS, v.119, pp.255 - 259-
dc.relation.isPartOfMICROBIAL PATHOGENESIS-
dc.citation.titleMICROBIAL PATHOGENESIS-
dc.citation.volume119-
dc.citation.startPage255-
dc.citation.endPage259-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaImmunology-
dc.relation.journalResearchAreaMicrobiology-
dc.relation.journalWebOfScienceCategoryImmunology-
dc.relation.journalWebOfScienceCategoryMicrobiology-
dc.subject.keywordPlusCYTOKINE PRODUCTION-
dc.subject.keywordPlusIN-VITRO-
dc.subject.keywordPlusPATHOGENESIS-
dc.subject.keywordPlusRELEASE-
dc.subject.keywordAuthorB. abortus-
dc.subject.keywordAuthorGallic acid-
dc.subject.keywordAuthorMacrophage-
dc.subject.keywordAuthorCytokines-
dc.subject.keywordAuthorProtection-
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