title: Metabolic and hematological consequences of dietary deoxynivalenol interacting with systemic Escherichia coli lipopolysaccharide.
abstract: Previous studies have shown that chronic oral deoxynivalenol (DON) exposure modulated Escherichia coli lipopolysaccharide (LPS)-induced systemic inflammation, whereby the liver was suspected to play an important role. Thus, a total of 41 barrows was fed one of two maize-based diets, either a DON-diet (4.59 mg DON/kg feed, n = 19) or a control diet (CON, n = 22). Pigs were equipped with indwelling catheters for pre- or post-hepatic (portal vs. jugular catheter) infusion of either control (0.9% NaCl) or LPS (7.5 µg/kg BW) for 1h and frequent blood sampling. This design yielded six groups: CON_CONjugular‑CONportal, CON_CONjugular‑LPSportal, CON_LPSjugular‑CONportal, DON_CONjugular‑CONportal, DON_CONjugular‑LPSportal and DON_LPSjugular‑CONportal. Blood samples were analyzed for blood gases, electrolytes, glucose, pH, lactate and red hemogram. The red hemogram and electrolytes were not affected by DON and LPS. DON-feeding solely decreased portal glucose uptake (p < 0.05). LPS-decreased partial oxygen pressure (pO₂) overall (p < 0.05), but reduced pCO₂ only in arterial blood, and DON had no effect on either. Irrespective of catheter localization, LPS decreased pH and base-excess (p < 0.01), but increased lactate and anion-gap (p < 0.01), indicating an emerging lactic acidosis. Lactic acidosis was more pronounced in the group DON_LPSjugular-CONportal than in CON-fed counterparts (p < 0.05). DON-feeding aggravated the porcine acid-base balance in response to a subsequent immunostimulus dependent on its exposure site (pre- or post-hepatic).
authors.affiliation: Institute of Animal Nutrition, Friedrich-Loeffler Institute (FLI), Federal Research Institute for Animal Health, Bundesallee 50, Braunschweig 38116, Germany. Erik.Bannert@fli.bund.de.
authors.forename: Erik
authors.initials: E
authors.lastname: Bannert
authors.affiliation: Institute of Animal Nutrition, Friedrich-Loeffler Institute (FLI), Federal Research Institute for Animal Health, Bundesallee 50, Braunschweig 38116, Germany. Tanja.Tesch@fli.bund.de.
authors.forename: Tanja
authors.initials: T
authors.lastname: Tesch
authors.affiliation: Institute of Animal Nutrition, Friedrich-Loeffler Institute (FLI), Federal Research Institute for Animal Health, Bundesallee 50, Braunschweig 38116, Germany. jeannette.kluess@fli.bund.de.
authors.forename: Jeannette
authors.initials: J
authors.lastname: Kluess
authors.affiliation: Institute of Animal Nutrition, Friedrich-Loeffler Institute (FLI), Federal Research Institute for Animal Health, Bundesallee 50, Braunschweig 38116, Germany. Jana.Frahm@fli.bund.de.
authors.forename: Jana
authors.initials: J
authors.lastname: Frahm
authors.affiliation: Institute of Animal Nutrition, Friedrich-Loeffler Institute (FLI), Federal Research Institute for Animal Health, Bundesallee 50, Braunschweig 38116, Germany. Susanne.Kersten@fli.bund.de.
authors.forename: Susanne
authors.initials: S
authors.lastname: Kersten
authors.affiliation: Institute of Anatomy, Otto-von-Guericke University Magdeburg, Leipziger Str. 44, Magdeburg 39120, Germany. stefan.kahlert@med.ovgu.de.
authors.forename: Stefan
authors.initials: S
authors.lastname: Kahlert
authors.affiliation: Institute of Anatomy, Otto-von-Guericke University Magdeburg, Leipziger Str. 44, Magdeburg 39120, Germany. lydia.renner@med.ovgu.de.
authors.forename: Lydia
authors.initials: L
authors.lastname: Renner
authors.affiliation: Institute of Anatomy, Otto-von-Guericke University Magdeburg, Leipziger Str. 44, Magdeburg 39120, Germany. hermann-josef.rothkoetter@med.ovgu.de.
authors.forename: Hermann-Josef
authors.initials: HJ
authors.lastname: Rothkötter
authors.affiliation: Institute of Animal Nutrition, Friedrich-Loeffler Institute (FLI), Federal Research Institute for Animal Health, Bundesallee 50, Braunschweig 38116, Germany. nicke@fli.bund.de.
authors.forename: Sven
authors.initials: S
authors.lastname: Dänicke
mesh_terms: D000136:Acid-Base Equilibrium / Q000187:drug effects; D000821:Animal Feed / Q000032:analysis*; D000818:Animals; D001784:Blood Gas Analysis; D001786:Blood Glucose / Q000032:analysis; D002245:Carbon Dioxide / Q000097:blood; D004032:Diet; D004906:Erythrocyte Count; D004926:Escherichia coli / Q000737:chemistry*; D005506:Food Contamination / Q000032:analysis*; D007249:Inflammation / Q000097:blood / Q000139:chemically induced; D008070:Lipopolysaccharides / Q000097:blood / Q000494:pharmacology*; D008297:Male; D034421:Sus scrofa; D014255:Trichothecenes / Q000097:blood / Q000494:pharmacology*; D014882:Water-Electrolyte Balance / Q000187:drug effects
chemical_list: D001786:Blood Glucose; D008070:Lipopolysaccharides; D014255:Trichothecenes; D002245:Carbon Dioxide; C007262:deoxynivalenol
keywords: E. coli lipopolysaccharides; blood gas; deoxynivalenol; endotoxin; glucose; inflammatory response; metabolism; sepsis; swine