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首页> 外文期刊>Biochemical Pharmacology >Lactobacillus rhamnosus GG supplementation modulates the gut microbiota to promote butyrate production, protecting against deoxynivalenol exposure in nude mice
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Lactobacillus rhamnosus GG supplementation modulates the gut microbiota to promote butyrate production, protecting against deoxynivalenol exposure in nude mice

机译：乳酸杆菌菌菌补充剂调节肠道微生物，促进丁酸盐的生产，保护裸鼠脱氧肾上腺素暴露

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Deoxynivalenol (DON) is the most common mycotoxin in grains, and DON exposure causes gastrointestinal inflammation and systemic immunosuppression. The immunosuppression caused by DON has raised serious concerns about whether it is safe to use probiotics in immunocompromised hosts. Gut microbiota remodeling by Lactobacillus is a potential effective strategy to prevent DON exposure. The athymic nude mice were chose as the model of immunocompromised animals. We tested the effect of the probiotic Lactobacillus rhamnosus GG (LGG) or Lactobacillus acidophilus (LA) supplementation on host protection against DON exposure and the underlying mechanisms in nude mice. DON exposure induced endoplasmic reticulum (ER) stress and impaired intestinal barrier function and microbiota, which were relieved by LGG supplementation but not LA supplementation. LGG supplementation significantly enhanced the intestinal barrier function, increased the body weight and the survival rate in nude mice that exposed to DON for two weeks. Furthermore, LGG supplementation modulated the gut microbiota by increasing the abundance of Bacteroidetes and the levels of the butyrate-producing genes But and Buk to promote butyrate production. Butyrate inhibited the IRE1 alpha/XBP1 signaling pathway to reduce DON-induced intestine injury. In conclusion, LGG supplementation modulated the gut microbiota to promote butyrate production, protecting against DON exposure in nude mice. Both LGG and butyrate show promise for use in protecting against DON exposure.
机译：脱氧性苯酚（Don）是谷物中最常见的霉菌毒素，唐暴露导致胃肠炎症和全身免疫抑制。由Don造成的免疫抑制提出了严重关切的是，在免疫功能性宿主中使用益生菌是安全的。乳酸杆菌改造的肠道微生物会改造是预防唐暴露的潜在有效策略。作为免疫环化动物的模型选择了无胸腺裸鼠。我们测试了益生菌乳杆菌菌株GG（Lactobacillus嗜酸乳杆菌（LAC）对宿主保护和裸鼠的潜在机制进行了补充的效果。 Don暴露诱导内质网（ER）应力和肠道势势障碍功能和微生物液，其通过LGG补充而释放但不是La补充。 LGG补充显着增强了肠道阻隔功能，增加了裸鼠的体重和裸鼠的存活率，暴露在唐持续两周。此外，通过增加诱导丁酸酯基因的丰度和丁酸酯的水平来调节肠道微生物，而不是促进丁酸酯的生产。丁酸盐抑制IS1α/ XBP1信号传导途径，以减少唐诱导的肠损伤。总之，LGG补充调节肠道微生物达促进丁酸盐生产，保护裸鼠唐暴露。 LGG和丁酸盐展示用于保护不暴露的承诺。

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