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      Modulation of Intestinal Functions Following Mycotoxin Ingestion: Meta-Analysis of Published Experiments in Animals

      review-article
      1 , 2 , 1 , *
      Toxins
      MDPI
      mycotoxin, gastrointestinal tract, nutrients, gut permeability, mucosal immunity, gut microbiota

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          Abstract

          Mycotoxins are secondary metabolites of fungi that can cause serious health problems in animals, and may result in severe economic losses. Deleterious effects of these feed contaminants in animals are well documented, ranging from growth impairment, decreased resistance to pathogens, hepato- and nephrotoxicity to death. By contrast, data with regard to their impact on intestinal functions are more limited. However, intestinal cells are the first cells to be exposed to mycotoxins, and often at higher concentrations than other tissues. In addition, mycotoxins specifically target high protein turnover- and activated-cells, which are predominant in gut epithelium. Therefore, intestinal investigations have gained significant interest over the last decade, and some publications have demonstrated that mycotoxins are able to compromise several key functions of the gastrointestinal tract, including decreased surface area available for nutrient absorption, modulation of nutrient transporters, or loss of barrier function. In addition some mycotoxins facilitate persistence of intestinal pathogens and potentiate intestinal inflammation. By contrast, the effect of these fungal metabolites on the intestinal microbiota is largely unknown. This review focuses on mycotoxins which are of concern in terms of occurrence and toxicity, namely: aflatoxins, ochratoxin A and Fusarium toxins. Results from nearly 100 published experiments ( in vitro, ex vivo and in vivo) were analyzed with a special attention to the doses used.

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          Most cited references91

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          Mycotoxin contamination of the feed supply chain: Implications for animal productivity and feed security

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            Worldwide occurrence of mycotoxins in commodities, feeds and feed ingredients

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              The food contaminant deoxynivalenol, decreases intestinal barrier permeability and reduces claudin expression.

              'The gastrointestinal tract represents the first barrier against food contaminants as well as the first target for these toxicants. Deoxynivalenol (DON) is a mycotoxin that commonly contaminates cereals and causes various toxicological effects. Through consumption of contaminated cereals and cereal products, human and pigs are exposed to this mycotoxin. Using in vitro, ex vivo and in vivo approaches, we investigated the effects of DON on the intestinal epithelium. We demonstrated that, in intestinal epithelial cell lines from porcine (IPEC-1) or human (Caco-2) origin, DON decreases trans-epithelial electrical resistance (TEER) and increases in a time and dose-dependent manner the paracellular permeability to 4 kDa dextran and to pathogenic Escherichia coli across intestinal cell monolayers. In pig explants treated with DON, we also observed an increased permeability of intestinal tissue. These alterations of barrier function were associated with a specific reduction in the expression of claudins, which was also seen in vivo in the jejunum of piglets exposed to DON-contaminated feed. In conclusion, DON alters claudin expression and decreases the barrier function of the intestinal epithelium. Considering that high levels of DON may be present in food or feed, consumption of DON-contaminated food/feed may induce intestinal damage and has consequences for human and animal health.
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                Author and article information

                Journal
                Toxins (Basel)
                Toxins (Basel)
                toxins
                Toxins
                MDPI
                2072-6651
                21 February 2013
                February 2013
                : 5
                : 2
                : 396-430
                Affiliations
                [1 ] Department of Animal Sciences, Purdue University, West Lafayette, IN 47907, USA; E-Mail: bgrenie@ 123456purdue.edu
                [2 ] Biomin Research Center, Tulln 3430, Austria
                Author notes
                [* ] Author to whom correspondence should be addressed; E-Mail: applegt@ 123456purdue.edu ; Tel.: +1-765-496-7769; Fax: +1-765-494-9346.
                Article
                toxins-05-00396
                10.3390/toxins5020396
                3640542
                23430606
                ece59906-7a8a-421c-b3f7-df1caad4c9cb
                © 2013 by the authors; licensee MDPI, Basel, Switzerland.

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                : 19 November 2012
                : 12 December 2012
                : 04 February 2013
                Categories
                Review

                Molecular medicine
                mycotoxin,gastrointestinal tract,nutrients,gut permeability,mucosal immunity,gut microbiota

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