Bovine TLR2 and TLR4 properly transduce signals from Staphylococcus aureus and E. coli, but S. aureus fails to both activate NF-kappaB in mammary epithelial cells and to quickly induce TNFalpha and interleukin-8 (CXCL8) expression in the udder.

@article{Yang2008BovineTA,
  title={Bovine TLR2 and TLR4 properly transduce signals from Staphylococcus aureus and E. coli, but S. aureus fails to both activate NF-kappaB in mammary epithelial cells and to quickly induce TNFalpha and interleukin-8 (CXCL8) expression in the udder.},
  author={Wei Yang and Holm Zerbe and Wolfram Petzl and Ronald Marco Brunner and Juliane G{\"u}nther and Christian Draing and Sonja von Aulock and Hans-Joachim Schuberth and H. -M. Seyfert},
  journal={Molecular immunology},
  year={2008},
  volume={45 5},
  pages={1385-97}
}
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 TNFalpha gene expression in… CONTINUE READING
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