@article{Yang2008Bovin-1117,
  year={2008},
  doi={10.1016/j.molimm.2007.09.004},
  title={Bovine TLR2 and TLR4 properly transduce signals from Staphylococcus aureus  and E. coli, but S. aureus fails to both activate NF-kB in mammary epithelial cells and to quickly induce TNFalpha and interleukin-8 (CXCL8) expression in the udder},
  number={5},
  volume={45},
  issn={0161-5890},
  journal={Molecular Immunology},
  pages={1385--1397},
  author={Yang, Wei and Zerbe, Holm and Petzl, Wolfram and Brunner, Ronald Marco and Günther, Juliane and Draing, Christian and Aulock, Sonja von and Schuberth, Hans-Joachim and Seyfert, Hans-Martin}
}

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    <dc:creator>Aulock, Sonja von</dc:creator>
    <dc:contributor>Aulock, Sonja von</dc:contributor>
    <dc:contributor>Schuberth, Hans-Joachim</dc:contributor>
    <dc:contributor>Seyfert, Hans-Martin</dc:contributor>
    <dc:creator>Seyfert, Hans-Martin</dc:creator>
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    <dc:contributor>Yang, Wei</dc:contributor>
    <dc:contributor>Draing, Christian</dc:contributor>
    <dc:language>eng</dc:language>
    <dc:contributor>Günther, Juliane</dc:contributor>
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    <dc:creator>Zerbe, Holm</dc:creator>
    <dc:contributor>Zerbe, Holm</dc:contributor>
    <dc:creator>Draing, Christian</dc:creator>
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    <dc:creator>Schuberth, Hans-Joachim</dc:creator>
    <dc:creator>Günther, Juliane</dc:creator>
    <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-03-23T09:06:16Z</dc:date>
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    <dc:contributor>Brunner, Ronald Marco</dc:contributor>
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    <dcterms:abstract xml:lang="eng">Staphylococcus aureus, but not E. coli  pathogens frequently cause subclinical, chronic infections of the mammary gland. We examined here, if inadequate activation of the bovine TLR2 and TLR4  pathogen receptors by ligands derived from S. aureus pathogens might contribute to molecular mechanisms underpinning the escape strategies from mammary immune defence of this pathogen. We show that infections with live E. coli, but not S. aureus pathogens induce strongly IL-8 and TNFα gene expression in the udders. Yet, preparations of heat-killed bacteria from both pathogens activate equally well bovine TLR2 and TLR4 receptors to induce NF-κB activation, as shown in the HEK293 reconstitution system of TLR-signal transduction. LTA prepared from the S. aureus strain used to infect the cows  activates the bovine TLR2 as strongly as the entire, heat-killed pathogen. Both pathogens induce in primary bovine mammary epithelial cells (pbMEC) IL-8  and TNFα gene expression, but S. aureus to less than 5% of the degree caused by E. coli. This impaired proinflammatory activation is paralleled by a complete lack of NF-κB activation in pbMEC by S. aureus or LTA. In contrast, E. coli and LPS activate strongly NF-κB in these cells. A large proportion of this activation is attributable to TLR-mediated signalling, since a dual transdominant negative DN-MyD88-DN-TRIF  factor blocks &gt;80% of the pathogen-related NF-κB activation in pbMEC. Our results prove that impaired binding of TLR-ligands from the pathogenic S. aureus strain are not the cause for the inadequate mammary immune response elicited by this pathogen. Rather, the pathogen causing subclinical mastitis impairs NF-κB activation in MEC thereby severely weakening the immune response in the udder.</dcterms:abstract>
    <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-03-23T09:06:16Z</dcterms:available>
    <dc:contributor>Petzl, Wolfram</dc:contributor>
    <dcterms:bibliographicCitation>Publ. in: Molecular Immunology 45 (2008), 5, pp. 1385-1397</dcterms:bibliographicCitation>
    <dc:creator>Yang, Wei</dc:creator>
    <dc:creator>Brunner, Ronald Marco</dc:creator>
    <dcterms:issued>2008</dcterms:issued>
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    <dcterms:title>Bovine TLR2 and TLR4 properly transduce signals from Staphylococcus aureus  and E. coli, but S. aureus fails to both activate NF-kB in mammary epithelial cells and to quickly induce TNFalpha and interleukin-8 (CXCL8) expression in the udder</dcterms:title>
    <dc:creator>Petzl, Wolfram</dc:creator>
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