• Login
    View Item 
    •   Home
    • Hospital Research
    • Munster
    • Cork University Hospital
    • View Item
    •   Home
    • Hospital Research
    • Munster
    • Cork University Hospital
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Map of Submissions

    Home Page
    UlsterN
    5081
    UlsterS
    5081
    Connacht
    1698
    Munster
    58
    Leinster
    466

    Browse

    All of Lenus, The Irish Health RepositoryCommunitiesTitleAuthorsDate publishedSubjectsThis CollectionTitleAuthorsDate publishedSubjects

    My Account

    LoginRegister

    About

    About LenusDirectory of Open Access JournalsOpen Access Publishing GuideNational Health Library & Knowledge ServiceGuide to Publishers' PoliciesFAQsTerms and ConditionsVision StatementORCID Unique identifiers for ResearchersHSE position statement on Open AccessNational Open Research Forum (NORF)Zenodo (European Open Research repository)

    Statistics

    Most Popular ItemsStatistics by CountryMost Popular Authors

    Bacterial lipoprotein-induced tolerance is reversed by overexpression of IRAK-1.

    • CSV
    • RefMan
    • EndNote
    • BibTex
    • RefWorks
    Authors
    Li, Chong Hui
    Liu, Jinghua
    An, Mingbang
    Redmond, H Paul
    Wang, Jiang Huai
    Affiliation
    Department of Academic Surgery, University College Cork (UCC)/National University of Ireland (NUI), Cork University Hospital, Cork, Ireland.
    Issue Date
    2012-03
    MeSH
    Bacterial Proteins
    Cell Line
    Gene Expression Regulation
    Humans
    Immune Tolerance
    Inflammation Mediators
    Interleukin-1 Receptor-Associated Kinases
    Interleukin-6
    Lipoproteins
    NF-kappa B
    Phosphorylation
    Sepsis
    Signal Transduction
    Toll-Like Receptor 2
    Transcriptional Activation
    Transgenes
    Tumor Necrosis Factor-alpha
    Show allShow less
    
    Metadata
    Show full item record
    Citation
    Bacterial lipoprotein-induced tolerance is reversed by overexpression of IRAK-1. 2012, 90 (3):314-20 Immunol. Cell Biol.
    Journal
    Immunology and cell biology
    URI
    http://hdl.handle.net/10147/239195
    DOI
    10.1038/icb.2011.37
    PubMed ID
    21537341
    Abstract
    Tolerance to bacterial cell wall components including bacterial lipoprotein (BLP) represents an essential regulatory mechanism during bacterial infection. Reduced Toll-like receptor 2 (TLR2) and IL-1 receptor-associated kinase 1 (IRAK-1) expression is a characteristic of the downregulated TLR signaling pathway observed in BLP-tolerised cells. In this study, we attempted to clarify whether TLR2 and/or IRAK-1 are the key molecules responsible for BLP-induced tolerance. Transfection of HEK293 cells and THP-1 cells with the plasmid encoding TLR2 affected neither BLP tolerisation-induced NF-κB deactivation nor BLP tolerisation-attenuated pro-inflammatory cytokine tumor necrosis factor alpha (TNF-α) production, indicating that BLP tolerance develops despite overexpression of TLR2 in these cells. In contrast, overexpression of IRAK-1 reversed BLP-induced tolerance, as transfection of IRAK-1 expressing vector resulted in a dose-dependent NF-κB activation and TNF-α release in BLP-tolerised cells. Furthermore, BLP-tolerised cells exhibited markedly repressed NF-κB p65 phosphorylation and impaired binding of p65 to several pro-inflammatory cytokine gene promoters including TNF-α and interleukin-6 (IL-6). Overexpression of IRAK-1 restored the nuclear transactivation of p65 at both TNF-α and IL-6 promoters. These results indicate a crucial role for IRAK-1 in BLP-induced tolerance, and suggest IRAK-1 as a potential target for manipulation of the TLR-mediated inflammatory response during microbial sepsis.
    Item Type
    Article
    Language
    en
    ISSN
    1440-1711
    ae974a485f413a2113503eed53cd6c53
    10.1038/icb.2011.37
    Scopus Count
    Collections
    Cork University Hospital

    entitlement

    Related articles

    • [The influence of over expression of interleukin-1 receptor-associated kinase 1 on bacterial lipoprotein-induced tolerance].
    • Authors: Li CH, Wang JJ, Gao LJ, Wang JH, Huang ZQ
    • Issue date: 2010 Jan
    • Bacterial lipoprotein-induced self-tolerance and cross-tolerance to LPS are associated with reduced IRAK-1 expression and MyD88-IRAK complex formation.
    • Authors: Li CH, Wang JH, Redmond HP
    • Issue date: 2006 Apr
    • Induction of bacterial lipoprotein tolerance is associated with suppression of toll-like receptor 2 expression.
    • Authors: Wang JH, Doyle M, Manning BJ, Di Wu Q, Blankson S, Redmond HP
    • Issue date: 2002 Sep 27
    • MicroRNA-146a is upregulated by and negatively regulates TLR2 signaling.
    • Authors: Quinn EM, Wang JH, O'Callaghan G, Redmond HP
    • Issue date: 2013
    • ST2 negatively regulates TLR2 signaling, but is not required for bacterial lipoprotein-induced tolerance.
    • Authors: Liu J, Buckley JM, Redmond HP, Wang JH
    • Issue date: 2010 May 15
    Health Library Ireland | Health Service Executive | Jervis House, Jervis Street | Republic of Ireland | Eircode: D01 W596
    lenus@hse.ie | Tel: +353-1-7786275
    DSpace software copyright © 2002-2017  DuraSpace
    Contact Us | Disclaimer
    Open Repository is a service operated by 
    Atmire NV
     

    Export search results

    The export option will allow you to export the current search results of the entered query to a file. Different formats are available for download. To export the items, click on the button corresponding with the preferred download format.

    By default, clicking on the export buttons will result in a download of the allowed maximum amount of items.

    To select a subset of the search results, click "Selective Export" button and make a selection of the items you want to export. The amount of items that can be exported at once is similarly restricted as the full export.

    After making a selection, click one of the export format buttons. The amount of items that will be exported is indicated in the bubble next to export format.