Lactiplantibacillus plantarum Lac16 Attenuates Enterohemorrhagic Escherichia coli O157:H7 Infection by Inhibiting Virulence Traits and Improving Intestinal Epithelial Barrier Function

Author:

Wang Baikui1ORCID,Zhou Yuanhao1,Wang Qi1,Xu Shujie1,Wang Fei1,Yue Min23ORCID,Zeng Zhonghua3,Li Weifen13

Affiliation:

1. Key Laboratory of Molecular Animal Nutrition of the Ministry of Education, Institute of Animal Nutrition and Feed Sciences, Zhejiang University College of Animal Sciences, Hangzhou 310058, China

2. Department of Veterinary Medicine, Institute of Preventive Veterinary Sciences, College of Animal Sciences, Zhejiang University, Hangzhou 310012, China

3. Nanjing Kangyou Biotechnology Co., Ltd., Nanjing 211316, China

Abstract

Large-scale use of antimicrobials in agriculture and medicine contributes to antibiotic residues in raw foods, the spread of antimicrobial resistance (AMR) and drug pollution, which seriously threatens human health and imposes significant economic burdens on society, suggesting the need for novel therapeutic options that prevent or control zoonoses. In this study, four probiotics were selected to assess their capability to alleviate pathogen-induced damage. Results showed that a simulated gastrointestinal juice and bile tolerated L. plantarum Lac16 with high lactic acid secretion can significantly inhibit the growth of multiple zoonotic pathogens. Lac16 also significantly inhibited the biofilm formation and mRNA expression of virulence traits (genes related to virulence, toxins, flagella biogenesis and motility, antibiotic resistance, biofilm formation and AI-2 quorum sensing) of enterohemorrhagic E. coli O157:H7 (EHEC). Furthermore, Lac16 and Lac26 significantly protected C. elegans against zoonotic pathogen-induced (EHEC, S. typhimurium, C. perfringens) deaths. Moreover, Lac16 significantly promoted epithelial repair and ameliorated lipopolysaccharide (LPS)-induced intestinal epithelial apoptosis and barrier dysfunction by activating the Wnt/β-catenin signaling pathway, and markedly reduced LPS-induced inflammatory responses by inhibiting the TLR4/MyD88 signaling pathway. The present results indicate that Lac16 attenuates enterohemorrhagic E. coli infection-induced damage by inhibiting key virulence traits of E. coli, promoting epithelial repair and improving intestinal epithelial barrier function, which may be mediated by the activated Wnt/β-catenin signaling pathway and the inhibited TLR4/MyD88 signaling pathway of the intestinal epithelium.

Funder

National Natural Science Foundation of China

Natural Science Foundation of Zhejiang province

District-level project for high-level innovative and entrepreneurial talents of “Zijinshan Talents Gaochun Plan”

Publisher

MDPI AG

Subject

General Medicine

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