Selenium-EnrichedPediococcus acidilacticiMRS-7 Alleviates Patulin-Induced Jejunum Injuries in Mice and Its Possible Mechanisms

Patulin (PAT) is a common mycotoxin. Oral ingestion of PAT could damage the intestinal mucosa. Both seleniumand probiotics can alleviate intestinal damage, but there are few reports on selenium-enriched probiotics. Here, we studied theprotective effects of a new selenium-enrichedPediococcus acidilacticiMRS-7 (SeP) on PAT-induced jejunum injuries in mice. Resultsshow that PAT induced jejunum injuries such as loss of crypts, ulceration of the mucosa, and intestinal epithelial barrier functionimpairment. However, SeP could protect against PAT-induced jejunum injuries and significantly inhibit the reduction of goblet cellnumbers. SeP could not only alleviate PAT-induced oxidative stress by decreasing malondialdehyde (MDA) and increasingsuperoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) levels in the jejunum tissues but also alleviatethe inflammatory response caused by PAT by reducing the levels of inflammatory factors (interleukin (IL)-6 snd IL-1 beta and tumornecrosis factor-alpha(TNF-alpha)) in the serum and jejunum tissues. In addition, SeP also inhibited the expression of nuclear factor-Kappa B(NF-Kappa B) and Toll-like receptor 4 (TLR-4), increased the expression of tight junction proteins (occludin, ZO-1, and claudin-1), andincreased the selenium content in the jejunum, thereby antagonizing the jejunum injuries caused by PAT exposure. Finally, SePrebalanced the intestinal microbiota and improved probiotic abundance such asTuricibacter,Bifidobacterium,Ileibacterium, andPediococcusin PAT-treated mice. These results support the possibility of SeP as a novel protective agent to mitigate the toxicity ofPAT.

Automated summary

This study investigated the protective effects of a selenium-enriched strain, SeP, on jejunum injuries induced by PAT. The results showed that SeP could alleviate PAT-induced intestinal damage and inflammation, as well as regulate the intestinal microbiota. These findings suggest that SeP may serve as a novel protective agent against the toxicity of PAT.