• Medientyp: E-Artikel
  • Titel: Does chronic dietary exposure to the mycotoxin deoxynivalenol affect the porcine hepatic transcriptome when an acute-phase response is initiated through first or second-pass LPS challenge of the liver?
  • Beteiligte: Dänicke, Sven; Heymann, Ann-Katrin; Oster, Michael; Wimmers, Klaus; Tesch, Tanja; Bannert, Erik; Bühler, Susanne; Kersten, Susanne; Frahm, Jana; Kluess, Jeannette; Kahlert, Stefan; Rothkötter, Hermann-Josef; Billenkamp, Fabian
  • Erschienen: SAGE Publications, 2021
  • Erschienen in: Innate Immunity
  • Sprache: Englisch
  • DOI: 10.1177/17534259211030563
  • ISSN: 1753-4259; 1753-4267
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  • Beschreibung: <jats:p> The sensitivity of pigs to deoxynivalenol (DON) might be increased by systemic inflammation (SI), which also has consequences for hepatic integrity. Liver lesions and a dys-regulated gene network might hamper hepatic handling and elimination of DON whereby the way of initiation of hepatic inflammation might play an additional role. First and second-pass exposure of the liver with LPS for triggering a SI was achieved by LPS infusion via pre- or post-hepatic venous route, respectively. Each infusion group was pre-conditioned either with a control diet (0.12 mg DON/kg diet) or with a DON-contaminated diet (4.59 mg DON/kg diet) for 4 wk. Liver transcriptome was evaluated at 195 min after starting infusions. DON exposure alone failed to modulate the mRNA expression significantly. However, pre- and post-hepatic LPS challenges prompted transcriptional responses in immune and metabolic levels. The mRNAs for B-cell lymphoma 2-like protein 11 as a key factor in apoptosis and IFN-γ released by T cells were clearly up-regulated in DON-fed group infused with LPS post-hepatically. On the other hand, mRNAs for nucleotide binding oligomerization domain containing 2, IFN-α and eukaryotic translation initiation factor 2α kinase 3 as ribosomal stress sensors were exclusively up-regulated in control pigs with pre-hepatic LPS infusion. These diverse effects were traced back to differences in TLR4 signalling. </jats:p>
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