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    Induction of bacterial lipoprotein tolerance is associated with suppression of toll-like receptor 2 expression.

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    Authors
    Wang, Jiang Huai
    Doyle, Majella
    Manning, Brian J
    Di Wu, Qiong
    Blankson, Siobhan
    Redmond, H Paul
    Affiliation
    Department of Academic Surgery, National University of Ireland, Cork University, Hospital, Cork, Ireland. jh.wang@ucc.ie
    Issue Date
    2012-02-03T15:10:27Z
    MeSH
    Antigens, CD14/biosynthesis/metabolism
    Bacterial Outer Membrane Proteins/*pharmacology
    Blotting, Western
    Cell Line
    Cell Nucleus/metabolism
    Cell Separation
    Culture Media, Serum-Free/pharmacology
    Cytokines/metabolism
    Down-Regulation
    *Drosophila Proteins
    Flow Cytometry
    Humans
    *Immune Tolerance
    Interleukin-6/metabolism
    Lipopolysaccharides/metabolism/*pharmacology
    Lipoproteins/*metabolism
    Luciferases/metabolism
    MAP Kinase Signaling System
    Membrane Glycoproteins/*biosynthesis/metabolism
    Microscopy, Fluorescence
    Monocytes/immunology/metabolism
    NF-kappa B/metabolism
    Phosphorylation
    Receptors, Cell Surface/*biosynthesis/metabolism
    Toll-Like Receptor 2
    Toll-Like Receptor 4
    Toll-Like Receptors
    Transfection
    Tumor Necrosis Factor-alpha/metabolism
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    Citation
    J Biol Chem. 2002 Sep 27;277(39):36068-75. Epub 2002 Jul 19.
    Journal
    The Journal of biological chemistry
    URI
    http://hdl.handle.net/10147/209033
    DOI
    10.1074/jbc.M205584200
    PubMed ID
    12133836
    Abstract
    Tolerance to bacterial cell wall components including lipopolysaccharide (LPS) may represent an essential regulatory mechanism during bacterial infection. Two members of the Toll-like receptor (TLR) family, TLR2 and TLR4, recognize the specific pattern of bacterial cell wall components. TLR4 has been found to be responsible for LPS tolerance. However, the role of TLR2 in bacterial lipoprotein (BLP) tolerance and LPS tolerance is unclear. Pretreatment of human THP-1 monocytic cells with a synthetic bacterial lipopeptide induced tolerance to a second BLP challenge with diminished tumor necrosis factor-alpha and interleukin-6 production, termed BLP tolerance. Furthermore, BLP-tolerized THP-1 cells no longer responded to LPS stimulation, indicating a cross-tolerance to LPS. Induction of BLP tolerance was CD14-independent, as THP-1 cells that lack membrane-bound CD14 developed tolerance both in serum-free conditions and in the presence of a specific CD14 blocking monoclonal antibody (MEM-18). Pre-exposure of THP-1 cells to BLP suppressed mitogen-activated protein kinase phosphorylation and nuclear factor-kappaB activation in response to subsequent BLP and LPS stimulation, which is comparable with that found in LPS-tolerized cells, indicating that BLP tolerance and LPS tolerance may share similar intracellular pathways. However, BLP strongly enhanced TLR2 expression in non-tolerized THP-1 cells, whereas LPS stimulation had no effect. Furthermore, a specific TLR2 blocking monoclonal antibody (2392) attenuated BLP-induced, but not LPS-induced, tumor necrosis factor-alpha and interleukin-6 production, indicating BLP rather than LPS as a ligand for TLR2 engagement and activation. More importantly, pretreatment of THP-1 cells with BLP strongly inhibited TLR2 activation in response to subsequent BLP stimulation. In contrast, LPS tolerance did not prevent BLP-induced TLR2 overexpression. These results demonstrate that BLP tolerance develops through down-regulation of TLR2 expression.
    Language
    eng
    ISSN
    0021-9258 (Print)
    0021-9258 (Linking)
    ae974a485f413a2113503eed53cd6c53
    10.1074/jbc.M205584200
    Scopus Count
    Collections
    Cork University Hospital

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