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

Lade...
Vorschaubild
Dateien
Zu diesem Dokument gibt es keine Dateien.
Datum
2008
Autor:innen
Yang, Wei
Zerbe, Holm
Petzl, Wolfram
Brunner, Ronald Marco
Draing, Christian
Schuberth, Hans-Joachim
Seyfert, Hans-Martin
Herausgeber:innen
Kontakt
ISSN der Zeitschrift
Electronic ISSN
ISBN
Bibliografische Daten
Verlag
Schriftenreihe
Auflagebezeichnung
ArXiv-ID
Internationale Patentnummer
Angaben zur Forschungsförderung
Projekt
Open Access-Veröffentlichung
Core Facility der Universität Konstanz
Gesperrt bis
Titel in einer weiteren Sprache
Publikationstyp
Zeitschriftenartikel
Publikationsstatus
Published
Erschienen in
Molecular Immunology. 2008, 45(5), pp. 1385-1397. ISSN 0161-5890. Available under: doi: 10.1016/j.molimm.2007.09.004
Zusammenfassung

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 >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.

Zusammenfassung in einer weiteren Sprache
Fachgebiet (DDC)
570 Biowissenschaften, Biologie
Schlagwörter
Bovine, Chemokines, Cow, Cytokines, HEK293
Konferenz
Rezension
undefined / . - undefined, undefined
Forschungsvorhaben
Organisationseinheiten
Zeitschriftenheft
Datensätze
Zitieren
ISO 690YANG, Wei, Holm ZERBE, Wolfram PETZL, Ronald Marco BRUNNER, Juliane GÜNTHER, Christian DRAING, Sonja von AULOCK, Hans-Joachim SCHUBERTH, Hans-Martin SEYFERT, 2008. 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. In: Molecular Immunology. 2008, 45(5), pp. 1385-1397. ISSN 0161-5890. Available under: doi: 10.1016/j.molimm.2007.09.004
BibTex
@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}
}
RDF
<rdf:RDF
    xmlns:dcterms="http://purl.org/dc/terms/"
    xmlns:dc="http://purl.org/dc/elements/1.1/"
    xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"
    xmlns:bibo="http://purl.org/ontology/bibo/"
    xmlns:dspace="http://digital-repositories.org/ontologies/dspace/0.1.0#"
    xmlns:foaf="http://xmlns.com/foaf/0.1/"
    xmlns:void="http://rdfs.org/ns/void#"
    xmlns:xsd="http://www.w3.org/2001/XMLSchema#" > 
  <rdf:Description rdf:about="https://kops.uni-konstanz.de/server/rdf/resource/123456789/1117">
    <dcterms:rights rdf:resource="https://rightsstatements.org/page/InC/1.0/"/>
    <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>
    <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dc:contributor>Yang, Wei</dc:contributor>
    <dc:contributor>Draing, Christian</dc:contributor>
    <dc:language>eng</dc:language>
    <dc:contributor>Günther, Juliane</dc:contributor>
    <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <bibo:uri rdf:resource="http://kops.uni-konstanz.de/handle/123456789/1117"/>
    <dc:creator>Zerbe, Holm</dc:creator>
    <dc:contributor>Zerbe, Holm</dc:contributor>
    <dc:creator>Draing, Christian</dc:creator>
    <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/52"/>
    <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>
    <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/>
    <dc:contributor>Brunner, Ronald Marco</dc:contributor>
    <foaf:homepage rdf:resource="http://localhost:8080/"/>
    <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/52"/>
    <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>
    <dc:rights>terms-of-use</dc:rights>
    <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>
  </rdf:Description>
</rdf:RDF>
Interner Vermerk
xmlui.Submission.submit.DescribeStep.inputForms.label.kops_note_fromSubmitter
Kontakt
URL der Originalveröffentl.
Prüfdatum der URL
Prüfungsdatum der Dissertation
Finanzierungsart
Kommentar zur Publikation
Allianzlizenz
Corresponding Authors der Uni Konstanz vorhanden
Internationale Co-Autor:innen
Universitätsbibliographie
Ja
Begutachtet
Diese Publikation teilen