Effects of gallic acid on signaling kinases in murine macrophages and immune modulation against Brucella abortus 544 infection in mice
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Reyes, Alisha Wehdnesday Bernardo | - |
dc.contributor.author | Arayan, Lauren Togonon | - |
dc.contributor.author | Hop, Huynh Tan | - |
dc.contributor.author | Tran Xuan Ngoc Huy | - |
dc.contributor.author | Vu, Son Hai | - |
dc.contributor.author | Min, WonGi | - |
dc.contributor.author | Lee, Hu Jang | - |
dc.contributor.author | Kim, Suk | - |
dc.date.accessioned | 2022-12-26T17:01:51Z | - |
dc.date.available | 2022-12-26T17:01:51Z | - |
dc.date.created | 2022-12-13 | - |
dc.date.issued | 2018-06 | - |
dc.identifier.issn | 0882-4010 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gnu/handle/sw.gnu/11623 | - |
dc.description.abstract | In 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.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD | - |
dc.subject | CYTOKINE PRODUCTION | - |
dc.subject | IN-VITRO | - |
dc.subject | PATHOGENESIS | - |
dc.subject | RELEASE | - |
dc.title | Effects of gallic acid on signaling kinases in murine macrophages and immune modulation against Brucella abortus 544 infection in mice | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Min, WonGi | - |
dc.contributor.affiliatedAuthor | Lee, Hu Jang | - |
dc.contributor.affiliatedAuthor | Kim, Suk | - |
dc.identifier.doi | 10.1016/j.micpath.2018.04.032 | - |
dc.identifier.scopusid | 2-s2.0-85046133810 | - |
dc.identifier.wosid | 000436385300036 | - |
dc.identifier.bibliographicCitation | MICROBIAL PATHOGENESIS, v.119, pp.255 - 259 | - |
dc.relation.isPartOf | MICROBIAL PATHOGENESIS | - |
dc.citation.title | MICROBIAL PATHOGENESIS | - |
dc.citation.volume | 119 | - |
dc.citation.startPage | 255 | - |
dc.citation.endPage | 259 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Immunology | - |
dc.relation.journalResearchArea | Microbiology | - |
dc.relation.journalWebOfScienceCategory | Immunology | - |
dc.relation.journalWebOfScienceCategory | Microbiology | - |
dc.subject.keywordPlus | CYTOKINE PRODUCTION | - |
dc.subject.keywordPlus | IN-VITRO | - |
dc.subject.keywordPlus | PATHOGENESIS | - |
dc.subject.keywordPlus | RELEASE | - |
dc.subject.keywordAuthor | B. abortus | - |
dc.subject.keywordAuthor | Gallic acid | - |
dc.subject.keywordAuthor | Macrophage | - |
dc.subject.keywordAuthor | Cytokines | - |
dc.subject.keywordAuthor | Protection | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
Gyeongsang National University Central Library, 501, Jinju-daero, Jinju-si, Gyeongsangnam-do, 52828, Republic of Korea+82-55-772-0533
COPYRIGHT 2022 GYEONGSANG NATIONAL UNIVERSITY LIBRARY. ALL RIGHTS RESERVED.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.