MYCOTOXINS ▶▶▶
inflammatory responses and pathogenic disorders in the animal (Figure 2).
Alteration of the intestinal barrier The mycotoxins DON, fumonisin, and T2 induce a reduction in the rate of epithelial cell proliferation and differentiation. This causes a decrease in the height and the surface of the intesti- nal villi, which in turn leads to a reduction in nutrient absorp- tion. Additionally, some nutrient transporters are inhibited by the action of mycotoxins, such as DON and T2, for example, negatively affecting the transport of glucose. Several studies indicate that mycotoxins such as aflatoxin B1, DON, fumonisin B1, ochratoxin A, and T2, can increase the permeability of the intestinal epithelium of poultry. This is mostly a consequence of the inhibition of protein synthesis. As a result, there is an increase in the passage of antigens into the bloodstream (e.g., bacteria, viruses and toxins). This increases the animal’s susceptibility to infectious enteric diseases. Moreover, the damage that mycotoxins cause to the intestinal barrier means that they are also being absorbed at a higher rate.
Impaired immune function The intestine is a very active immune site where several im- muno-regulatory mechanisms simultaneously defend the body from harmful agents. Immune cells are affected by my- cotoxins through the initiation of apoptosis, the inhibition or stimulation of cytokines and the induction of oxidative stress. Studies demonstrate that aflatoxin, DON, fumonisin, T2, and zearalenone interact with the intestinal immune system in such a manner that the animal’s susceptibility to viral and bacterial infections increases. Moreover, by increasing their faecal elimination, the horizontal transmission of pathogens is extended. In poultry production one of the most severe enteric prob- lems of bacterial origin is necrotic enteritis which is caused by Clostridium perfringens toxins. Any agent capable of disrupt- ing the gastrointestinal epithelium – e.g., mycotoxins such as
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DON, T2 and ochratoxin – promotes the development of ne- crotic enteritis. The inhibition of the intestinal immune sys- tem, caused by mycotoxins such as aflatoxin, DON, and T2, also contributes to the development of this disease.
Alteration of the microflora The gastrointestinal tract is home to a diverse community of bacteria, fungi, protozoa, and viruses which line the walls of the distal part of the intestine. This microbiota prevents the growth of pathogenic bacteria through competitive exclusion and the secretion of natural antimicrobial compounds, vola- tile fatty acids and organic acids. Recent studies on the effect of various mycotoxins on the intestinal microbiota show that DON and other trichothecenes favour the colonization of coli- form bacteria in pigs. DON and ochratoxin A also induce a greater invasion of Salmonella and their translocation to the bloodstream and vital organs in birds and pigs – even at non-cytotoxic concentrations. It is known that fumonisin B1 may induce changes in the balance of sphingolipids at the cellular level, including for gastrointestinal cells. This facili- tates the adhesion of pathogenic bacteria, population in- crease and prolongs infections, as has been shown in the case of E. coli. From the perspective of human health, the coloniza- tion of the intestine of food-producing animals with patho- genic strains of E. coli and Salmonella is of particular concern. Mycotoxin exposure may well increase the transmission of these pathogens, posing a risk to human health.
Interaction with bacterial toxins When mycotoxins induce changes in the intestinal microbio- ta, this can lead to an increase in the endotoxin concentration in the intestinal lumen. Endotoxins or lipopolysaccharides (LPS) are cell wall fragments of Gram-negative bacteria. They are released during bacterial cell death, growth and division. Hence endotoxins are always present in the intestine, even in healthy animals. Endotoxins promote the release of several cytokines that induce an enhanced immune response,
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