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Pediococcus acidilactici P25 Protected Caenorhabditis elegans against Enterotoxigenic Escherichia coli K88 Infection and Transcriptomic Analysis of Its Potential Mechanisms

文献类型： 外文期刊

作者： Tan, Keqin 1 ; Deng, Dun 1 ; Ma, Xianyong 1 ; Cui, Yiyan 1 ; Tian, Zhimei 1 ;

作者机构： 1.Guangdong Acad Agr Sci, Guangdong Engn Technol Res Ctr Anim Meat Qual & S, Guangdong Key Lab Anim Breeding & Nutr,State Key, Inst Anim Sci,Minist Agr,Key Lab Anim Nutr & Feed, Guangzhou 510640, Peoples R China

期刊名称：BIOMED RESEARCH INTERNATIONAL （ 影响因子：3.411； 五年影响因子：3.62 ）

ISSN： 2314-6133

年卷期： 2020 年 2020 卷

页码：

收录情况： SCI

摘要： Enterotoxigenic Escherichia coli (ETEC) K88 is a zoonotic pathogen. Previous studies have shown that lactic acid bacteria (LAB) have great potential in promoting health and resisting pathogenic infections; however, relatively little research has been done on the Pediococcus genus of LAB. This study is aimed at exploring the mechanisms imparted by Pediococcus acidilactici P25 against ETEC K88 in Caenorhabditis elegans. The probiotic performance of P25 was investigated in vitro. Colonization of K88 in the intestinal tract of C. elegans and abundance of enterotoxin genes were measured. In addition, the transcriptome of C. elegans infected by K88 was analyzed. The result showed that P25 possessed the ability to produce acid, as well as high tolerances to acidic and high bile salt concentrations. Coculture revealed that the growth of ETEC K88 was significantly inhibited by the presence of P25. The median survival of C. elegans fed P25 was 2 days longer than the group infected with K88 alone (P<0.01). At the same time, the number of colonizing K88 and the abundances of estB and elt were reduced by up to 71.70% and 2.17 times, respectively, by P25. Transcriptome data indicated that P25 affected expression of genes relative to innate immune response and upregulated the abundance of genes in multiple pathways of C. elegans, including peroxisome, longevity, and mitogen-activated protein kinase (MAPK) pathways. These results demonstrated that in the presence of P25, K88 colonization and their expression of enterotoxin genes were reduced. This was accomplished through the alteration of environmental parameters (pH and bile salt) as well as through the promotion of the innate immune response processes, increased longevity, and increased antipathogenic bacteria-related pathways. This work highlights the potential application of P. acidilactici P25 as a probiotic resistant to ETEC K88.

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