Porcine milk exosomes play an important role in mother-infant communication. Deoxynivalenol (DON) is a toxin which causes serious damage to the animal intestinal mucosa. Our previous study showed porcine milk exosomes facilitate mice intestine development, but the effects of these exosomes to antagonize DON toxicity is unclear. Our in vivo results showed that milk exosomes attenuated DON-induced damage on the mouse body weight and intestinal epithelium growth. In addition, these exosomes could reverse DON-induced inhibition on cell proliferation and tight junction proteins (TJs) formation and reduce DON-induced cell apoptosis. In vitro, exosomes up-regulated the expression of miR-181a, miR-30c, miR-365-5p and miR-769-3p in IPEC-J2 cells and then down-regulated the expression of their targeting genes in p53 pathway, ultimately attenuating DON-induced damage by promoting cell proliferation and TJs and by inhibiting cell apoptosis. In conclusion, porcine milk exosomes could protect the intestine against DON damage, and these protections may take place through the miRNAs in exosomes. These results indicated that the addition of miRNA-enriched exosomes to feed or food could be used as a novel preventative measure for necrotizing enterocolitis.
Keywords: Deoxynivalenol; Porcine milk exosomes; Proliferation and apoptosis; Tight junctions; miRNA.
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