MicroRNA-146a is upregulated by and negatively regulates TLR2 signaling

Show simple item record

dc.contributor.author Quinn, Edel M.
dc.contributor.author Wang, Jiang Huai
dc.contributor.author O'Callaghan, Grace
dc.contributor.author Redmond, H. Paul
dc.contributor.editor Bereswill, Stefan
dc.date.accessioned 2013-07-04T08:30:48Z
dc.date.available 2013-07-04T08:30:48Z
dc.date.copyright 2013
dc.date.issued 2013-04-29
dc.identifier.citation Quinn EM, Wang JH, O’Callaghan G, Redmond HP (2013) MicroRNA-146a Is Upregulated by and Negatively Regulates TLR2 Signaling. PLoS ONE 8(4): e62232. doi:10.1371/journal.pone.0062232 en
dc.identifier.volume 8 en
dc.identifier.issued 4 en
dc.identifier.startpage e62232 en
dc.identifier.issn 1932-6203
dc.identifier.uri http://hdl.handle.net/10468/1158
dc.identifier.doi 10.1371/journal.pone.0062232
dc.description.abstract TLR signaling is a crucial component of the innate immune response to infection. MicroRNAs (miRNAs) have been shown to be upregulated during TLR signaling. Specifically, microRNA-146a (miR-146a) plays a key role in endotoxin tolerance by downregulating interleukin-1 receptor-associated kinase 1 (IRAK-1). The aim of this study was to assess the role of miR-146a in the TLR2 signaling and development of bacterial lipoprotein (BLP) self-tolerance and cross-tolerance to bacteria. Expression of miR-146a increased in a dose- and time-dependent manner in BLP-stimulated human THP-1 promonocytic cells. In BLP-tolerised cells miR-146a was even further upregulated in response to BLP re-stimulation (p,0.001). Restimulation of BLP-tolerised cells with heat-killed gram-negative Salmonella typhimurium (S. typhimurium), but not grampositive Staphylococcus aureus (S. aureus), led to significant overexpression of miR-146a (p,0.05). Transfection of naive cells with a miR-146a mimic substantially suppressed TNF-a production (p,0.05). Furthermore, overexpression of miR-146a resulted in strong reduction in IRAK-1 and phosphorylated IkBa expression in naive and S. typhimurium-stimulated THP-1 cells. Collectively, miR-146a is upregulated in response to BLP and bacterial stimulation in both naive and BLP-tolerised cells. Overexpression of miR-146a induces a state analogous to tolerance in BLP-stimulated cells and therefore may represent a future target for exogenous modulation of tolerance during microbial infection and sepsis en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher PLOS ONE en
dc.rights ©2013 Quinn et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. en
dc.rights.uri http://creativecommons.org/licenses/by/2.5/ en
dc.subject TLR signaling en
dc.subject MicroRNAs en
dc.subject Immune response to infection en
dc.title MicroRNA-146a is upregulated by and negatively regulates TLR2 signaling en
dc.type Article (peer-reviewed) en
dc.internal.authorurl http://www.ucc.ie/en/surgery/staff/researchstaff/jhwang/ en
dc.internal.authorcontactother Jiang Huai Wang, Department of Academic Surgery, University College Cork, Cork University Hospital, Cork, Ireland en
dc.internal.availability Full text available en
dc.description.version Published Version en
dc.description.status Peer reviewed en
dc.identifier.journaltitle PLOS One en
dc.internal.IRISemailaddress jh.wang@ucc.ie en


Files in this item

This item appears in the following Collection(s)

Show simple item record

©2013 Quinn et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Except where otherwise noted, this item's license is described as ©2013 Quinn et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
This website uses cookies. By using this website, you consent to the use of cookies in accordance with the UCC Privacy and Cookies Statement. For more information about cookies and how you can disable them, visit our Privacy and Cookies statement