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Conference Paper: The role of c-Myc in phagocytosis of mycobacteria in human macrophages

TitleThe role of c-Myc in phagocytosis of mycobacteria in human macrophages
Authors
KeywordsPediatrics
Issue Date2013
PublisherMedcom Limited. The Journal's web site is located at http://www.hkjpaed.org/index.asp
Citation
The 2013 Joint Annual Scientific Meeting of The Hong Kong Paediatric Society and Hong Kong Paediatric Nurses Association, Hong Kong, 8 September 2013. In Hong Kong Journal of Paediatrics (New series), 2013, v. 18 n. 4, p. 254 How to Cite?
AbstractMycobacterium tuberculosis is an intracellular pathogen and the causative agent of the disease tuberculosis. Macrophages are the major immunocytes to initiate host immunity against mycobacteria. Among the multiple strategies employ by macrophages to defence against mycobacteria, phagocytosis is the first step. Throughphagocytosis, macrophages could not only clear the pathogens from infection sites, but also present antigens derived from the engulfed bacteria to lymphoid cells. c-Myc is a transcription factor that regulates a variety of target genes. It can form a complex with Max and bind to the enhancer box sequences of the promoter to mediate the transcription. Recently, our group revealed that c-Myc has a potential role in regulating the antimicrobial responses in macrophages. Here, we further revealed that c-Myc may play a positive role in phagocytosis and contribute to host defense to mycobacteria. Pretreatment of c-Myc inhibitor, 10058-F4, could significantly reduce the amount of mycobacteria internalised by macrophages. The acidification of phagolysosome in mycobacteria infected macrophages was also inhibited by 10058-F4. Further investigation showed that macrophages phagocytose mycobacteria in a PI3K/Akt independent pathway. And the action of c-Myc inhibitor does not affect the expression levels of Rho family GTPases. However, we found that 10058-F4 could significantly inhibit phorsphorylation of ERK1/2 kinase, which has been indicated to play a role in FcR mediated phagocytosis in macrophage. In conclusion, c-Myc may play a role in phagocytosis of mycobacteria through regulating phorsphorylation of ERK1/2.
DescriptionPoster Presentation (Doctor’s Session)
This journal issue contain proceedings of the Congress
Persistent Identifierhttp://hdl.handle.net/10722/206046
ISSN
2015 Impact Factor: 0.194
2015 SCImago Journal Rankings: 0.123

 

DC FieldValueLanguage
dc.contributor.authorWang, Len_US
dc.contributor.authorLing, WLen_US
dc.contributor.authorLi, JCBen_US
dc.contributor.authorLau, ASY-
dc.date.accessioned2014-10-20T11:47:22Z-
dc.date.available2014-10-20T11:47:22Z-
dc.date.issued2013en_US
dc.identifier.citationThe 2013 Joint Annual Scientific Meeting of The Hong Kong Paediatric Society and Hong Kong Paediatric Nurses Association, Hong Kong, 8 September 2013. In Hong Kong Journal of Paediatrics (New series), 2013, v. 18 n. 4, p. 254en_US
dc.identifier.issn1013-9923-
dc.identifier.urihttp://hdl.handle.net/10722/206046-
dc.descriptionPoster Presentation (Doctor’s Session)-
dc.descriptionThis journal issue contain proceedings of the Congress-
dc.description.abstractMycobacterium tuberculosis is an intracellular pathogen and the causative agent of the disease tuberculosis. Macrophages are the major immunocytes to initiate host immunity against mycobacteria. Among the multiple strategies employ by macrophages to defence against mycobacteria, phagocytosis is the first step. Throughphagocytosis, macrophages could not only clear the pathogens from infection sites, but also present antigens derived from the engulfed bacteria to lymphoid cells. c-Myc is a transcription factor that regulates a variety of target genes. It can form a complex with Max and bind to the enhancer box sequences of the promoter to mediate the transcription. Recently, our group revealed that c-Myc has a potential role in regulating the antimicrobial responses in macrophages. Here, we further revealed that c-Myc may play a positive role in phagocytosis and contribute to host defense to mycobacteria. Pretreatment of c-Myc inhibitor, 10058-F4, could significantly reduce the amount of mycobacteria internalised by macrophages. The acidification of phagolysosome in mycobacteria infected macrophages was also inhibited by 10058-F4. Further investigation showed that macrophages phagocytose mycobacteria in a PI3K/Akt independent pathway. And the action of c-Myc inhibitor does not affect the expression levels of Rho family GTPases. However, we found that 10058-F4 could significantly inhibit phorsphorylation of ERK1/2 kinase, which has been indicated to play a role in FcR mediated phagocytosis in macrophage. In conclusion, c-Myc may play a role in phagocytosis of mycobacteria through regulating phorsphorylation of ERK1/2.-
dc.languageengen_US
dc.publisherMedcom Limited. The Journal's web site is located at http://www.hkjpaed.org/index.asp-
dc.relation.ispartofHong Kong Journal of Paediatrics (New series)en_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectPediatrics-
dc.titleThe role of c-Myc in phagocytosis of mycobacteria in human macrophagesen_US
dc.typeConference_Paperen_US
dc.identifier.emailWang, L: vickyw@hku.hken_US
dc.identifier.emailLing, WL: durandal@hku.hken_US
dc.identifier.emailLi, JCB: jamesli@hku.hken_US
dc.identifier.emailLau, ASY: asylau@hku.hk-
dc.identifier.authorityLi, JCB=rp00496en_US
dc.identifier.authorityLau, ASY=rp00474en_US
dc.description.naturepublished_or_final_version-
dc.identifier.hkuros241318en_US
dc.identifier.hkuros241325-
dc.identifier.volume18-
dc.identifier.issue4-
dc.identifier.spage254-
dc.identifier.epage254-
dc.publisher.placeHong Kong-

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