PLoS ONE (Jan 2011)

The mycotoxin deoxynivalenol potentiates intestinal inflammation by Salmonella typhimurium in porcine ileal loops.

  • Virginie Vandenbroucke,
  • Siska Croubels,
  • An Martel,
  • Elin Verbrugghe,
  • Joline Goossens,
  • Kim Van Deun,
  • Filip Boyen,
  • Arthur Thompson,
  • Neil Shearer,
  • Patrick De Backer,
  • Freddy Haesebrouck,
  • Frank Pasmans

DOI
https://doi.org/10.1371/journal.pone.0023871
Journal volume & issue
Vol. 6, no. 8
p. e23871

Abstract

Read online

Background and aimsBoth deoxynivalenol (DON) and nontyphoidal salmonellosis are emerging threats with possible hazardous effects on both human and animal health. The objective of this study was to examine whether DON at low but relevant concentrations interacts with the intestinal inflammation induced by Salmonella Typhimurium.MethodologyBy using a porcine intestinal ileal loop model, we investigated whether intake of low concentrations of DON interacts with the early intestinal inflammatory response induced by Salmonella Typhimurium.ResultsA significant higher expression of IL-12 and TNFα and a clear potentiation of the expression of IL-1β, IL-8, MCP-1 and IL-6 was seen in loops co-exposed to 1 µg/mL of DON and Salmonella Typhimurium compared to loops exposed to Salmonella Typhimurium alone. This potentiation coincided with a significantly enhanced Salmonella invasion in and translocation over the intestinal epithelial IPEC-J2 cells, exposed to non-cytotoxic concentrations of DON for 24 h. Exposure of Salmonella Typhimurium to 0.250 µg/mL of DON affected the bacterial gene expression level of a limited number of genes, however none of these expression changes seemed to give an explanation for the increased invasion and translocation of Salmonella Typhimurium and the potentiated inflammatory response in combination with DON.ConclusionThese data imply that the intake of low and relevant concentrations of DON renders the intestinal epithelium more susceptible to Salmonella Typhimurium with a subsequent potentiation of the inflammatory response in the gut.