Abstract
Mycotoxins, which are widely found in feed ingredients and human food, can exert harmful effects on animals and pose a serious threat to human health. As the first barrier against external pollutants, the intestinal mucosa is protected by a mechanical barrier, chemical barrier, immune barrier, and biological barrier. Firstly, mycotoxins can disrupt the mechanical barrier function of the intestinal mucosa, by destroying the morphology and tissue integrity of the intestinal epithelium. Secondly, mycotoxins can cause changes in the composition of mucin monosaccharides and the expression of intestinal mucin, which in turn affects mucin function. Thirdly, mycotoxins can cause damage to the intestinal mucosal immune barrier function. Finally, the microbiotas of animals closely interact with ingested mycotoxins. Based on existing research, this article reviews the effects of mycotoxins on the intestinal mucosal barrier and its mechanisms.
Highlights
Mycotoxins are secondary metabolites produced by filamentous fungi or molds during grain growth, harvesting, storage and processing, including deoxynivalenol (DON), aflatoxin B1 (AFB1), zearalenone (ZEA), ochratoxin A (OTA), T-2 toxin and fumonisin B (FBs) [1]
Pinton and colleagues [44] used human goblet cells (HT29-16E) and porcine small intestine explants as experimental subjects and found that MUC1, MUC2, and MUC3 mRNA and protein expression were observed after exposure to the mycotoxin DON for 48 h, and effects on the intestinal mucosal barrier were observed
We inferred that when the intestinal tract was damaged by mycotoxins, the expression of mucin mRNA increased by upregulating the secretion of antimicrobial peptides, thereby enhancing the chemical barrier function of the intestinal mucosa
Summary
Mycotoxins are secondary metabolites produced by filamentous fungi or molds during grain growth, harvesting, storage and processing, including deoxynivalenol (DON), aflatoxin B1 (AFB1), zearalenone (ZEA), ochratoxin A (OTA), T-2 toxin and fumonisin B (FBs) [1]. Diesing and coworkers [36] showed that after 2000 ng/mL DON was applied to the polarized epithelial cells of porcine small intestinal origin (IPEC-1 and IPEC-J2), the expression of tight junction protein ZO-1 decreased, and the intestinal mechanical barrier integrity was destroyed. Pinton and colleagues [44] used human goblet cells (HT29-16E) and porcine small intestine explants as experimental subjects and found that MUC1, MUC2, and MUC3 mRNA and protein expression were observed after exposure to the mycotoxin DON for 48 h, and effects on the intestinal mucosal barrier were observed. We inferred that when the intestinal tract was damaged by mycotoxins, the expression of mucin mRNA increased by upregulating the secretion of antimicrobial peptides, thereby enhancing the chemical barrier function of the intestinal mucosa. The results of Hongbo’s work [49] showed that the antimicrobial peptide CWA could improve the self-repair ability of damaged intestinal epithelial cells and the barrier function of the intestinal mucosa
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