Isolation, identification and safety evaluation of OTA-detoxification strain Pediococcus acidilactici NJB421 and its effects on OTA-induced toxicity in mice.

Ochratoxin A (OTA) is a potent mycotoxin found in foods and feeds, posing a health risk to animals and humans. Biological detoxification of OTA is considered a promising method, and some bacteria and fungi which can degrade OTA are isolated. However, research on safety and alleviating toxic effects are scarce. This study aims to isolate OTA-detoxification probiotics from natural samples and evaluate their safety and protective effects in mice. Here, a new OTA-detoxification strain named Pediococcus acidilactici NJB421 (P. acidilactici NJB421) was isolated from cow manure, which exhibited a removal rate of OTA at 48.53% for 48 h. P. acidilactici NJB421 exhibited high temperature resistance, acid tolerance, 0.3% bile salt and 1.4% trypsin resistance. The safety evaluation showed that P. acidilactici NJB421 at 2 × 108 CFU/per mouse had no abnormalities in body weight, organ indices, ALT, AST and ALP activities, BUN, CRE and TP contents. And P. acidilactici NJB421 alleviated the decreases in body weight, organ indices and small intestinal length, and alleviated intestinal injury, liver injury and kidney injury. These results suggest P. acidilactici NJB421 is safe and has protection against OTA poisoning, which provides a new OTA-detoxification strain for livestock and food industries.

Crucial Function of Caveolin-1 in Deoxynivalenol-Induced Enterotoxicity by Activating ROS-Dependent NLRP3 Inflammasome-Mediated Pyroptosis.

Deoxynivalenol (DON) is one of the most pervasive contaminating mycotoxins in grain, and exposure to DON is known to cause acute and chronic intestinal damage. As the gut is the most important target organ of DON, it is essential to identify the pivotal molecules involved in DON-induced enterotoxicity as well as the potential regulatory mechanisms. In the present study, we found that DON treatment dramatically decreased the jejunal villus height and increased the crypt depth in mice. DON exposure induced oxidative stress and NLRP3 inflammasome activation while increasing the levels of pyroptosis-related factors GSDMD, ASC, Caspase-1 P20, and IL-1ß and inflammatory cytokines IL-18, TNF-α, and IL-6. In vitro, 0.5-2 µM DON caused cytotoxicity and oxidative stress, as well as NLRP3-mediated pyroptosis in IPEC-J2 cells. Furthermore, DON treatment substantially improved the expression of Caveolin-1 (Cav-1) in vitro and in vivo. Interestingly, Cav-1 knockdown effectively attenuated DON-induced oxidative stress and NLRP3-mediated pyroptosis in IPEC-J2 cells. Meanwhile, treatment with the antioxidant NAC significantly alleviated DON-induced cytotoxicity and pyroptosis in IPEC-J2 cells. Likewise, after inhibiting NLRP3 inflammasome activation with the inhibitor MCC950, DON-induced cytotoxicity, pyroptosis, and inflammatory response were attenuated. However, NLRP3 inhibition did not affect Cav-1 expression. In conclusion, our study demonstrated that pyroptosis may be an underlying mechanism in DON-induced intestinal injury, and Cav-1 plays a pivotal role in DON-induced pyroptosis via regulating oxidative stress, which suggests a novel strategy to overcome DON-induced enterotoxicity.