Deoxynivalenol exposure induces liver damage in mice: Inflammation and immune responses, oxidative stress, and protective effects of Lactobacillus rhamnosus GG. (October 2021)

• Record Type: Journal Article
• Authors: Bai, Yongsong; Ma, Kaidi; Li, Jibo; Li, Jianping; Bi, Chongpeng; Shan, Anshan
• Is Part Of: Food and chemical toxicology. Volume 156(2021)
• Publication Date: 2021-10
• Subjects: Mycotoxins -- Probiotics -- Inflammatory cytokines -- TLR4/NF-κB -- Keap1-Nrf2; Toxicology -- Periodicals; Food poisoning -- Periodicals; Food Poisoning -- Periodicals; Toxicology -- Periodicals; Toxicologie -- Périodiques; Intoxications alimentaires -- Périodiques; Food poisoning; Toxicology; Periodicals; Electronic journals; 615.9
• DOI: 10.1016/j.fct.2021.112514
• Languages: English
• ISSNs: 0278-6915

Abstract

Abstract: Deoxynivalenol (DON), one of the most common environmental pollutants, substantially affects human and animal health. Much attention has been paid to the ability of probiotics to modulate inflammation and immune responses. In this work, the toxic effects of DON on the liver and the protective effects of Lactobacillus rhamnosus GG (LGG) were investigated. We treated mice with oral gavage of DON (2.4 mg/kg bw/day), LGG (1 × 10 9 CFU/mouse/day) or both for 28 days. The results showed that DON triggered liver inflammation, reflected by pathological changes and liver function damage but LGG oral administration significantly attenuated these changes. Notably, DON treatment activated the TLR4/NF-κB signaling pathway which contribute to produce inflammatory cytokines, but oral administration of LGG inhibited all the effects of DON. DON treatment can also induce oxidative stress and activate Keap1-Nrf2 signaling pathway, leading to the activation of Nrf2 and the downstream genes, while LGG treatment can improve the antioxidant capacity of liver and protected mice from DON injury. In conclusion, LGG was able to negate the detrimental effects of DON on the liver and may contribute as a potential dietary intervention strategy to reduce mycotoxicity. Graphical abstract: Image 1 Highlights: Deoxynivalenol exposure to mice leads to liver function abnormalities. The TLR4/NF-κB signaling was involved in deoxynivalenol-induced liver inflammation. Deoxynivalenol can cause oxidative stress and activate Keap1-Nrf2 signaling pathway. Lactobacillus rhamnosus GG protected against deoxynivalenol-induced liver damage.