A chronic oral exposure of pigs with deoxynivalenol partially prevents the acute effects of lipopolysaccharides on hepatic histopathology and blood clinical chemistry

Lipopolysaccharides (LPS), a cell wall component of gram-negative bacteria, and deoxynivalenol (DON), a prevalent Fusarium-derived contaminant of cereal grains, are each reported to have detrimental effects on the liver. A potentiating toxic effect of the combined exposure was reported previously in a mouse model and hepatocytes in vitro, but not in swine as the most DON-susceptible species. Thus, pigs were fed either a control diet (CON) or a Fusarium contaminated diet (DON, 3.1 mg DON/kg diet) for 37 days. At day 37 control pigs were infused for 1 h either with physiological saline (CON_CON), 100 μg/kg BW DON (CON_DON), 7.5 μg/kg BW LPS (CON_LPS), or both toxins (CON_DON/LPS) and Fusarium-pigs with saline (DON_CON) or 7.5 μg/kg BW LPS (DON_LPS). Blood samples were taken before and after infusion (−30, +30, +60, +120, and +180 min) for clinical blood chemistry. Pigs were sacrificed at +195 min and liver histopathology was performed. LPS resulted in higher relative liver weight (p < 0.05), portal, periportal and acinar inflammation (p < 0.05), haemorrhage (p < 0.01) and pathological bilirubin levels (CON_CON 1.0 μmol/L vs. CON_LPS 5.4 μmol/L, CON_DON/LPS 8.3 μmol/L; p < 0.001). DON feeding alleviated effects of LPS infusion on histopathology and blood chemistry to control levels, whereas DON infusion alone had no impact.

► Systemic deoxynivalenol alone does not alter hepatic morphology and function.
► Escherichia coli LPS induces hepatic inflammation and haemorrhage and impairs liver function.
► Deoxynivalenol feeding alleviates detrimental effects of a subsequent LPS challenge.