Lactiplantibacillus plantarum ELF051 Alleviates Antibiotic-Associated Diarrhea by Regulating Intestinal Inflammation and Gut Microbiota
文献类型： 外文期刊
作者： Liang, Wei 1 ; Gao, Yansong 2 ; Zhao, Yujuan 2 ; Gao, Lei 2 ; Zhao, Zijian 2 ; He, Zhongmei 1 ; Li, Shengyu 2 ;
作者机构： 1.Jilin Agr Univ, Coll Chinese Med Mat, Changchun 130118, Peoples R China
2.Jilin Acad Agr Sci, Inst Agrofood Technol, 1363 Sheng-Tai St, Changchun 130033, Peoples R China
关键词： Antibiotic-associated diarrhea; Gut microbiota; Intestinal inflammation; Lactiplantibacillus plantarum; Short-chain fatty acids
期刊名称：PROBIOTICS AND ANTIMICROBIAL PROTEINS （ 影响因子：4.9； 五年影响因子：5.4 ）
ISSN： 1867-1306
年卷期： 2023 年
页码：
收录情况： SCI
摘要： Probiotics are widely recognized for their ability to prevent and therapy antibiotic-associated diarrhea (AAD). This study was designed to evaluate Lactiplantibacillus plantarum ELF051 ability to prevent colon inflammation and its effect on gut microbial composition in a mouse model of AAD. The mice were intragastrically administered triple antibiotics for 7 days and then subjected to L. plantarum ELF051 for 14 days. The administration of L. plantarum ELF051 ameliorated the pathological changes in the colon tissue, downregulated interleukin (IL)-1 beta and tumor necrosis factor (TNF)-alpha, and upregulated IL-10, and increased the intestinal short-chain fatty acids (SCFAs) level. Lactiplantibacillus plantarum ELF051 also regulated the Toll-like receptor/myeloid differentiation primary response 88/nuclear factor kappa light chain enhancer of activated B cells (TLR4/MyD88/NF-.B) and the phosphatidylinositol 3-kinase/protein kinase B/ NF-kappa B (PI3K/AKT/ NF-kappa B) inflammatory signaling pathways. 16S rRNA analyses showed that L. plantarum ELF051 increased the abundance and diversity of gut bacteria, restoring gut microbiota imbalance. A Spearman's rank correlation analysis showed that lactobacilli are closely associated with inflammatory markers and SCFAs. This work demonstrated that L. plantarum ELF051 can attenuate antibiotic-induced intestinal inflammation in a mouse AAD model by suppressing the pro-inflammatory response and modulating the gut microbiota.
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