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

Cells. 2023 May 21;12(10):1438. doi: 10.3390/cells12101438.

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.

Keywords: Lactiplantibacillus plantarum; Wnt/β-catenin pathway; barrier dysfunction; enterohemorrhagic E. coli O157:H7; epithelial damage.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Caenorhabditis elegans
  • Escherichia coli O157* / genetics
  • Humans
  • Lipopolysaccharides*
  • Myeloid Differentiation Factor 88
  • Toll-Like Receptor 4
  • Virulence / genetics

Substances

  • Lipopolysaccharides
  • Toll-Like Receptor 4
  • Myeloid Differentiation Factor 88

Grants and funding

The present research was supported by National Natural Science Foundation of China (No. 32072766, 31672460 and 31472128); Natural Science Foundation of Zhejiang province (No. LZ20C170002 and No. 2006C12086); District-level project for high-level innovative and entrepreneurial talents of the “Zijinshan Talents Gaochun Plan” (No. 202100677).