File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Conference Paper: MicroRNAs mediated-regulation of mycobacteria-induced cytokines production

TitleMicroRNAs mediated-regulation of mycobacteria-induced cytokines production
Authors
Issue Date2013
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/cytokine
Citation
The 11th Joint Meeting ofJoint Annual Meeting of the International Cytokine Society (ICS) and the International Society for Interferon and Cytokine Research (ISICR), San Francisco, California, 29 September-3 October 2013. In Cytokine, 2013, v. 63 n. 3, p. 245, abstract no. 9 How to Cite?
AbstractTuberculosis (TB) is generally acquired through inhalation of airborne droplets containing Mycobacterium tuberculosis (Mtb). Macrophages are one of the pivotal cells in innate immunity against mycobacteria. Mycobacteria activate macrophages to produce proinflammatory cytokines such as TNF-α which controls Mtb infection. The cytokine is crucial for granuloma formation, induction of macrophage apoptosis and production of chemokines to recruit cells in tuberculosis. TNF-α biosynthesis is known to be controlled at the transcriptional and post-transcriptional levels. Emerging studies have shown that microRNAs (miRNAs), a family of single stranded, non-coding, short RNAs, act as post-transcriptional regulators of gene expressions. MiRNA-mediated regulations are essential in various developmental and cellular processes including tumor development and immune responses. MiRNAs regulate innate immunity and shape adaptive immunity. They target mRNAs of toll-like receptors (TLR), cellular signaling molecules, transcription factors or cytokines as to regulate the immunity. In this study, it was shown that various miRNAs were induced in primary human macrophages by Bacille Calmette-Guerin (BCG), a vaccine for TB. MiR-1303, which has not been shown to have function, was found to regulate BCG-induced TNF-α mRNA and protein production. It was shown that by knock-down of miR-1303, BCG-induced TNF-α protein expression was upregulated. In contrast, overexpression of miR-1303 can suppress the TNF-α protein expression. Additionally, it was demonstrated that miR-1303 could control levels of phosphorylated extracellular-signal-regulated kinase (ERK) and phosphorylated p38 mitogen-activated protein kinase (p38 MAPK). Further studies on the mechanisms of the regulation will be required and the studies will delineate how miRNAs manipulate immune responses to mycobacteria infection. Copyright © 2013 Published by Elsevier Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/206044
ISSN
2015 Impact Factor: 2.94
2015 SCImago Journal Rankings: 1.294
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorAu, KYen_US
dc.contributor.authorLi, CBen_US
dc.contributor.authorLau, ASYen_US
dc.date.accessioned2014-10-20T11:47:22Z-
dc.date.available2014-10-20T11:47:22Z-
dc.date.issued2013en_US
dc.identifier.citationThe 11th Joint Meeting ofJoint Annual Meeting of the International Cytokine Society (ICS) and the International Society for Interferon and Cytokine Research (ISICR), San Francisco, California, 29 September-3 October 2013. In Cytokine, 2013, v. 63 n. 3, p. 245, abstract no. 9en_US
dc.identifier.issn1043-4666-
dc.identifier.urihttp://hdl.handle.net/10722/206044-
dc.description.abstractTuberculosis (TB) is generally acquired through inhalation of airborne droplets containing Mycobacterium tuberculosis (Mtb). Macrophages are one of the pivotal cells in innate immunity against mycobacteria. Mycobacteria activate macrophages to produce proinflammatory cytokines such as TNF-α which controls Mtb infection. The cytokine is crucial for granuloma formation, induction of macrophage apoptosis and production of chemokines to recruit cells in tuberculosis. TNF-α biosynthesis is known to be controlled at the transcriptional and post-transcriptional levels. Emerging studies have shown that microRNAs (miRNAs), a family of single stranded, non-coding, short RNAs, act as post-transcriptional regulators of gene expressions. MiRNA-mediated regulations are essential in various developmental and cellular processes including tumor development and immune responses. MiRNAs regulate innate immunity and shape adaptive immunity. They target mRNAs of toll-like receptors (TLR), cellular signaling molecules, transcription factors or cytokines as to regulate the immunity. In this study, it was shown that various miRNAs were induced in primary human macrophages by Bacille Calmette-Guerin (BCG), a vaccine for TB. MiR-1303, which has not been shown to have function, was found to regulate BCG-induced TNF-α mRNA and protein production. It was shown that by knock-down of miR-1303, BCG-induced TNF-α protein expression was upregulated. In contrast, overexpression of miR-1303 can suppress the TNF-α protein expression. Additionally, it was demonstrated that miR-1303 could control levels of phosphorylated extracellular-signal-regulated kinase (ERK) and phosphorylated p38 mitogen-activated protein kinase (p38 MAPK). Further studies on the mechanisms of the regulation will be required and the studies will delineate how miRNAs manipulate immune responses to mycobacteria infection. Copyright © 2013 Published by Elsevier Ltd.-
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/cytokine-
dc.relation.ispartofCytokineen_US
dc.rightsNOTICE: this is the author’s version of a work that was accepted for publication in <Journal title>. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in PUBLICATION, [VOL#, ISSUE#, (DATE)] DOI#-
dc.titleMicroRNAs mediated-regulation of mycobacteria-induced cytokines productionen_US
dc.typeConference_Paperen_US
dc.identifier.emailAu, KY: aukinyi@graduate.hku.hken_US
dc.identifier.emailLi, CB: jamesli@graduate.hku.hken_US
dc.identifier.emailLau, ASY: asylau@hku.hken_US
dc.identifier.authorityLi, CB=rp00496en_US
dc.identifier.authorityLau, ASY=rp00474en_US
dc.identifier.doi10.1016/j.cyto.2013.06.012-
dc.identifier.hkuros241320en_US
dc.identifier.volume63-
dc.identifier.issue3-
dc.identifier.spage245, abstract no. 9-
dc.identifier.epage245, abstract no. 9-
dc.identifier.isiWOS:000324013700021-
dc.publisher.placeUnited Kingdom-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats