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

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.

The progression of deoxynivalenol-induced growth suppression in nursery pigs and the potential of an algae-modified montmorillonite clay to mitigate these effects12

“…These effects are known to have the greatest impact on rapidly dividing cells, such as epithelial and immune cells in the gastrointestinal tract (GIT; Van De Walle et al, 2010). Thus, DON contamination causes compromised barrier function by decreasing the expression of tight junction proteins (Van De Walle et al, 2010;Pinton et al, 2012) and can increase the susceptibility of the GIT to bacterial infections (Grenier and Applegate, 2013). Exposure to DON also decreases the rate of epithelial cell division, resulting in flattened intestinal villi and reducing the absorptive surface area for nutrient uptake (Bracarense et al, 2012).…”

“…Conceivably, these effects indicate that the toxicity of DON might be dramatically greater if exposure were to occur alongside bacterial infection. Nonetheless, the modulation of these digestive and immune functions by DON does not always affect animal growth parameters (Grenier and Applegate, 2013).…”

“…While vomiting occurs at high concentrations (Forsyth et al, 1977;Pestka et al, 1987), most reports agree that realistic DON levels (1 to 5 mg/kg) primarily decrease feed intake (Friend et al, 1984;Patience et al, 2014). Deoxynivalenol also reduces intestinal absorption (Grenier and Applegate, 2013) and stimulates and suppresses the immune system (Rotter et al, 1996;Pestka et al, 2004). The severity seems to be dose-dependent, and fluctuations may be related to contradictory feed efficiency effects (Etienne and Waché, 2008).…”

Immunohistochemical evaluation of apoptosis and proliferation in the mucous membrane of selected uterine regions in pre-pubertal bitches exposed to low doses of zearalenone

“…This could take place during exposure to low levels of undesirable substances in feedstuffs, and it can produce a U-shaped or a reverse U-shaped non-monotonic dose response (NMDR) (hormesis; Calabrese 2005). In reference to the NMDR hypothesis, an ambiguous correlation between the dose and the response implies that the risks (clinical symptoms or laboratory results) associated with high doses cannot be directly and unambiguously extrapolated to low doses (Grenier and Applegate 2013).…”

Mycotoxins in Poultry

“…FUMzyme (carboxyl-esterase) was further developed and tested in swine for gastrointestinal detoxiication of FUM by cleaving the tricarballylic side chains of FUM leading to the non-toxic metabolite hydrolyzed FUM (HFB1) [93].…”