Abstract |
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.
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Authors | Sven Dänicke, Ann-Katrin Heymann, Michael Oster, Klaus Wimmers, Tanja Tesch, Erik Bannert, Susanne Bühler, Susanne Kersten, Jana Frahm, Jeannette Kluess, Stefan Kahlert, Hermann-Josef Rothkötter, Fabian Billenkamp |
Journal | Innate immunity
(Innate Immun)
Vol. 27
Issue 5
Pg. 388-408
(07 2021)
ISSN: 1753-4267 [Electronic] United States |
PMID | 34338001
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Lipopolysaccharides
- Mycotoxins
- Trichothecenes
- deoxynivalenol
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Topics |
- Acute-Phase Reaction
(genetics, metabolism)
- Animal Feed
- Animals
- Chemical and Drug Induced Liver Injury
(genetics, metabolism)
- Diet
(adverse effects)
- Dietary Exposure
- Food Contamination
- Lipopolysaccharides
(metabolism)
- Liver
(physiology)
- Mycotoxins
- Swine
- Transcriptome
- Trichothecenes
(toxicity)
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