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    The induction of macrophage gene expression by LPS predominantly utilizes Myd88-independent signaling cascades

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    Authors
    Bjorkbacka, Harry
    Fitzgerald, Katherine A.
    Huet, Francois
    Li, Xiaoman
    Gregory, James A.
    Lee, Melinda
    Ordija, Christine M.
    Dowley, Nicole E.
    Golenbock, Douglas T.
    Freeman, Mason W.
    UMass Chan Affiliations
    Department of Medicine, Division of Infectious Diseases and Immunology
    Document Type
    Journal Article
    Publication Date
    2004-09-16
    Keywords
    Adaptor Proteins, Signal Transducing
    Animals
    Antigens, Differentiation
    Cells, Cultured
    DNA-Binding Proteins
    Escherichia coli K12
    Gene Expression Profiling
    Gene Expression Regulation
    Genetic Markers
    Humans
    Inflammation
    Interferon Regulatory Factor-3
    Kidney
    Lipopolysaccharides
    Macrophage Activation
    Macrophages
    Mice
    Mice, Inbred C57BL
    Microarray Analysis
    Myeloid Differentiation Factor 88
    NF-kappa B
    Proteins
    Receptors, Immunologic
    Signal Transduction
    Toll-Like Receptor 4
    Transcription Factors
    Transfection
    Immunology and Infectious Disease
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    Abstract
    Myeloid differentiation protein-88 (MyD88) is a signal adaptor protein required for cytokine production following engagement of Toll-like receptors (TLRs) by their cognate ligands. Activation of both TLR-3 and TLR-4, however, can engage signaling events independent of MyD88 expression. The relative importance of these MyD88-dependent and -independent signaling pathways in the macrophage response to lipopolysaccharide (LPS) is unknown. Here we define these events using microarray expression profiling of LPS-stimulated macrophages taken from MyD88-null and wild-type mice. Of the 1,055 genes found to be LPS responsive, only 21.5% were dependent on MyD88 expression, with MyD88-independent genes constituting 74.7% of the genetic response. This MyD88-independent gene expression was predominantly transcriptionally regulated, as it was unaffected by cycloheximide blockade of new protein synthesis. A previously undescribed group of LPS-regulated genes (3.8%), whose induction or repression was significantly greater in the absence of MyD88, was also identified by these studies. The regulation of these genes suggested that MyD88 could serve as a molecular brake, constraining gene activity in a subset of LPS-responsive genes. The findings generated with LPS stimulation were recapitulated by exposure of macrophages to live Escherichia coli. These expression-profiling studies redefine the current dogma of TLR-4 signaling and establish that MyD88, although essential for some of the best-characterized macrophage responses to LPS, is not required for the regulation of the majority of genes engaged by macrophage exposure to endotoxin or live bacteria.
    Source
    Physiol Genomics. 2004 Nov 17;19(3):319-30. Epub 2004 Sep 14. Link to article on publisher's site
    DOI
    10.1152/physiolgenomics.00128.2004
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/35262
    PubMed ID
    15367722
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1152/physiolgenomics.00128.2004
    Scopus Count
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