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The food contaminant fumonisin B1 reduces the maturation of porcine CD11R1+ intestinal dendritic cells, resulting in a reduced efficiency of oral immunisation and a prolonged intestinal ETEC infection

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Abstract
Consumption of food or feed contaminated with fumonisin B1 (FB1), a mycotoxin produced by Fusarium verticillioides, leads to disease in humans and animals. This mycotoxin reduces the efficiency of parenteral vaccinations, indicating that ingestion of FB1-contaminated food suppresses the systemic immune system. This study was conducted to elucidate the mechanisms by which FB1 exerts its immunosuppressive effects on the intestinal immune system. Piglets were used as a model species for humans since their gastrointestinal tracts are very similar both on an anatomical and physiological level. The animals were orally exposed to a low dose of FB1 (1 mg/kg body weight) for 10 days which did not result in any clinical signs. However, when compared to control animals, FB1-exposed animals demonstrated a prolonged excretion of the porcine-specific enteropathogen F4+ enterotoxigenic E. coli (F4+ ETEC) following infection. Upon oral immunisation with purified F4 fimbriae, FB1 exposure reduced the intestinal antigen-specific immune response as compared to control animals. Further analyses to elucidate the mechanisms behind these observations revealed a reduced expression of IL-12p40 mRNA by intestinal immune cells. Since this cytokine is mainly secreted by antigen presenting cells, we analysed the effects of FB1 on small intestinal CD11R1+ lamina propria dendritic cells (LPDC). These CD11R1+ LPDC matured in response to stimulation with the ETEC-derived virulence factors, F4 fimbriae and flagellin, indicating that this intestinal DC subset is involved in the induction of protective immunity. However, in vivo exposure of piglets to FB1 impaired the functional maturation of F4 fimbriae- and flagellin-stimulated CD11R1+ LPDC as evidenced by a decreased upregulation of MHCII and CD80/86 and a reduced T cell stimulatory capacity. These results indicate an FB1-mediated reduction of in vivo DC maturation and stress the need to reduce exposure of animals and humans to FB1 in order to enhance the efficacy of vaccination programs.

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Chicago
Devriendt, Bert, Mélanie Gallois, Frank Verdonck, Yann Wache, Diane Bimczok, Isabelle Oswald, Bruno Goddeeris, and Eric Cox. 2011. “The Food Contaminant Fumonisin B1 Reduces the Maturation of Porcine CD11R1+ Intestinal Dendritic Cells, Resulting in a Reduced Efficiency of Oral Immunisation and a Prolonged Intestinal ETEC Infection.” In ECMIS, Abstracts.
APA
Devriendt, B., Gallois, M., Verdonck, F., Wache, Y., Bimczok, D., Oswald, I., Goddeeris, B., et al. (2011). The food contaminant fumonisin B1 reduces the maturation of porcine CD11R1+ intestinal dendritic cells, resulting in a reduced efficiency of oral immunisation and a prolonged intestinal ETEC infection. ECMIS, Abstracts. Presented at the ECMIS 2011 : Escherichia coli and the Mucosal Immune System : interaction, modulation and vaccination.
Vancouver
1.
Devriendt B, Gallois M, Verdonck F, Wache Y, Bimczok D, Oswald I, et al. The food contaminant fumonisin B1 reduces the maturation of porcine CD11R1+ intestinal dendritic cells, resulting in a reduced efficiency of oral immunisation and a prolonged intestinal ETEC infection. ECMIS, Abstracts. 2011.
MLA
Devriendt, Bert, Mélanie Gallois, Frank Verdonck, et al. “The Food Contaminant Fumonisin B1 Reduces the Maturation of Porcine CD11R1+ Intestinal Dendritic Cells, Resulting in a Reduced Efficiency of Oral Immunisation and a Prolonged Intestinal ETEC Infection.” ECMIS, Abstracts. 2011. Print.
@inproceedings{1957045,
  abstract     = {Consumption of food or feed contaminated with fumonisin B1 (FB1), a mycotoxin produced by Fusarium verticillioides, leads to disease in humans and animals. This mycotoxin reduces the efficiency of parenteral vaccinations, indicating that ingestion of FB1-contaminated food suppresses the systemic immune system. This study was conducted to elucidate the mechanisms by which FB1 exerts its immunosuppressive effects on the intestinal immune system. Piglets were used as a model species for humans since their gastrointestinal tracts are very similar both on an anatomical and physiological level. The animals were orally exposed to a low dose of FB1 (1 mg/kg body weight) for 10 days which did not result in any clinical signs. However, when compared to control animals, FB1-exposed animals demonstrated a prolonged excretion of the porcine-specific enteropathogen F4+ enterotoxigenic E. coli (F4+ ETEC) following infection. Upon oral immunisation with purified F4 fimbriae, FB1 exposure reduced the intestinal antigen-specific immune response as compared to control animals. Further analyses to elucidate the mechanisms behind these observations revealed a reduced expression of IL-12p40 mRNA by intestinal immune cells. Since this cytokine is mainly secreted by antigen presenting cells, we analysed the effects of FB1 on small intestinal CD11R1+ lamina propria dendritic cells (LPDC). These CD11R1+ LPDC matured in response to stimulation with the ETEC-derived virulence factors, F4 fimbriae and flagellin, indicating that this intestinal DC subset is involved in the induction of protective immunity. However, in vivo exposure of piglets to FB1 impaired the functional maturation of F4 fimbriae- and flagellin-stimulated CD11R1+ LPDC as evidenced by a decreased upregulation of MHCII and CD80/86 and a reduced T cell stimulatory capacity. These results indicate an FB1-mediated reduction of in vivo DC maturation and stress the need to reduce exposure of animals and humans to FB1 in order to enhance the efficacy of vaccination programs.},
  author       = {Devriendt, Bert and Gallois, M{\'e}lanie  and Verdonck, Frank and Wache, Yann and Bimczok, Diane and Oswald, Isabelle and Goddeeris, Bruno and Cox, Eric},
  booktitle    = {ECMIS, Abstracts},
  language     = {eng},
  location     = {Ghent, Belgium},
  title        = {The food contaminant fumonisin B1 reduces the maturation of porcine CD11R1+ intestinal dendritic cells, resulting in a reduced efficiency of oral immunisation and a prolonged intestinal ETEC infection},
  year         = {2011},
}