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<p>Deoxynivalenol (DON), a prevalent mycotoxin in food and feed, induces gastrointestinal and liver damage. The potential probiotic <i>Bacillus velezensis</i> may mitigate DON toxicity, though its precise mechanisms remain unknown. Our study demonstrates that <i>B. velezensis</i> WMCC10514 effectively survives and degrades DON within simulated gastrointestinal fluid. Fluorescently labeled WMC10514-GFP colonized murine intestines and persisted in simulated intestinal fluid (SIF), confirming its colonization capacity. In <i>vivo</i>, WMCC10514 alleviated DON-induced anorexia, restored murine growth, and reduced liver injury. Furthermore, the strain elevated ZO-1 and Occludin expression, enhanced intestinal barrier integrity and reduced DON accumulation in host tissues. Integrated transcriptomic and microbiome analyses revealed that the strain suppressed TLR4/NF-κB pathway activation in the intestine and liver, increased <i>Lactobacillus</i> abundance, restored SCFAs level, and modulated liver energy metabolism. These findings elucidate <i>B. velezensis</i>’s role in mitigating mycotoxin toxicity through gut microbiota-driven regulation of the gut-liver axis.</p><p></p>

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Bacillus velezensis mitigates deoxynivalenol-induced intestinal inflammation and liver injury via modulating the gut microbiota

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月14日

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  • Xinyi Huang,
  • Bowen Xu,
  • Ying Lei,
  • Haixiong Qin,
  • Jia Zheng,
  • Yan Xu,
  • Dong Zhao,
  • Jian Su,
  • Jingyi Li,
  • Jiayuan Zhao

摘要

Deoxynivalenol (DON), a prevalent mycotoxin in food and feed, induces gastrointestinal and liver damage. The potential probiotic Bacillus velezensis may mitigate DON toxicity, though its precise mechanisms remain unknown. Our study demonstrates that B. velezensis WMCC10514 effectively survives and degrades DON within simulated gastrointestinal fluid. Fluorescently labeled WMC10514-GFP colonized murine intestines and persisted in simulated intestinal fluid (SIF), confirming its colonization capacity. In vivo, WMCC10514 alleviated DON-induced anorexia, restored murine growth, and reduced liver injury. Furthermore, the strain elevated ZO-1 and Occludin expression, enhanced intestinal barrier integrity and reduced DON accumulation in host tissues. Integrated transcriptomic and microbiome analyses revealed that the strain suppressed TLR4/NF-κB pathway activation in the intestine and liver, increased Lactobacillus abundance, restored SCFAs level, and modulated liver energy metabolism. These findings elucidate B. velezensis’s role in mitigating mycotoxin toxicity through gut microbiota-driven regulation of the gut-liver axis.