Novel mechanism by which extracellular vesicles derived from Lactobacillus murinus alleviates deoxynivalenol-induced intestinal barrier disruption
文献类型： 外文期刊
作者： Fan, Jinping 1 ; Zhang, Yuhan 1 ; Zuo, Minyu 1 ; Ding, Shixuan 1 ; Li, Jingjing 1 ; Feng, Shengkai 1 ; Xiao, Yingping 2 ; Tao, Shiyu 1 ;
作者机构： 1.Huazhong Agr Univ, Coll Anim Sci & Technol, Wuhan 430070, Peoples R China
2.Zhejiang Acad Agr Sci, Inst Agroprod Safety & Nutr, State Key Lab Managing Biot & Chem Threats Qual &, Hangzhou 310021, Peoples R China
关键词： Deoxynivalenol; Lactobacillus murinus; Extracellular vesicles; Macrophage; Gut barrier
期刊名称：ENVIRONMENT INTERNATIONAL （ 影响因子：10.3； 五年影响因子：11.1 ）
ISSN： 0160-4120
年卷期： 2024 年 185 卷
页码：
收录情况： SCI
摘要： Deoxynivalenol (DON) is a common environmental pollutant that poses a serious health risk to humans worldwide. This study was aim to explore whether gut microbiota is involved in DON-induced intestinal toxicity as well as to reveal effect of probiotics derived from gut microbiota in protecting intestinal barrier and to elucidate mechanism. We found that DON caused disturbed gut microbiota, particularly Lactobacillus murinus (L. murinus) deficiency. DON enhanced M1 macrophage polarization and decreased tight junction protein expression. Microbiota transplantation experiments showed that transfer of DON-disrupted microbiota to healthy mice resulted in delivery of DON-induced intestinal toxicity. Besides, DON lost its damaging effect on macrophage and intestinal barrier in antibiotic-treated mice. Further intervention experiments revealed that L. murinus induce macrophage conversion from M1 to M2 phenotype through secreted extracellular vesicles (EVs) to alleviate DON-induced intestinal barrier disruption. Mechanistically, EVs activate TLR2 to promote M2 macrophage polarization and release IL-10, which in turn enhances intestinal barrier function. Upon successful translation of its efficacy into clinical practice, EVs created from L. murinus could be a novel possible treatment strategy for DON-induced gut disease.
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