epithelium, several types of highly specialised cells are in- volved in epithelial regeneration, nutrient absorption, innate defence, transport of immunoglobulins and immune surveil- lance. The selective barrier function is maintained due to the formation of complex networks of proteins that link adjacent cells and seal the intercellular space. Besides, the intestinal epithelium is covered with mucus produced by goblet cells, which isolates its surface preventing the adhesion of patho- gens to the enterocytes (intestinal absorptive cells). Due to its dual involvement in digestive and immune processes, the in- testinal epithelium plays a pivotal role in the animal’s overall health. Importantly, the epithelium is directly exposed to the entire load of ingested mycotoxins. Hence their effects can be problematic even at low concentrations.
Attack on the intestinal epithelium Most mycotoxins are absorbed in the proximal part of the gastrointestinal tract (Table 1). This absorption can be high, as in the case of aflatoxins (~90%), but also very limited, as in the case of fumonisins (<1%); moreover, it depends on the species. Importantly, a significant portion of unabsorbed tox- ins remains in the lumen of the gastrointestinal tract. Some of the mycotoxins that enter the intestinal lumen can be bio-transformed into less toxic compounds by the action of certain bacteria. This action, however, predominantly hap- pens in the large intestine – therefore, no detoxification takes place before absorption in the upper parts of the GIT. Some of the absorbed mycotoxins can also re-enter the intestine, reaching the cells from the basolateral side via the blood- stream. They can also re-enter through enterohepatic circula-
tion (the circulation of substances between the liver and small intestine). Both actions increase the gastrointestinal tract’s overall exposure to the toxins. The damaging impact of mycotoxins on the intestinal epithelium initially occurs through: • A decrease in protein synthesis, which reduces barrier and immune function.
• Increased oxidative stress at the cellular level, which leads to lipid peroxidation, affecting cell membranes.
• Changes in gene expression and the production of chemical messengers (cytokines), with effects on the immune system and cellular growth and differentiation.
• The induction of programmed cell death (apoptosis), affect- ing the reposition of immune and absorptive cells.
Importantly, studies based on realistic mycotoxin challenges show that the mycotoxin levels necessary to trigger these processes are lower than the levels reported as safe by EFSA, the Food Safety Agency of the European Union. The ultimate consequences range from diminished nutrient absorption to
Figure 2 - Mycotoxins’ impact on the GIT and consequences for monogastric animals.
Inhibition of protein synthesis
Oxidative stress Changes in gene expression
Induction of apoptosis
Alteration of intestinal barrier morphology and functionality
Impaired immune function
Alteration of intestinal microflora
Interaction with bacterial toxins
Diminished nutrient absoprtion
Inflammatory response
Pathogenic disorders
Animal feed is often contami- nated with two or more myco- toxins, making it important for an anti-mycotoxin agent to be ef- fective against a wide range of different mycotoxins.
PHOTO: HANS BANUS
▶ POULTRY WORLD | No. 6, 2020
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Mycotoxins Basic mechanisms
Intermediary processes
Final results
Decrease in health, productivity, and welfare
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