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<p>Lactic acid bacteria (LAB) have anti-inflammatory, hypolipidemic and hypoglycemic properties, as well as the ability to maintain intestinal flora balance, but are susceptible to inactivation by environmental stresses. To solve the above issues, improving biofilm formation has been applied to enhance bacterial resistance to environmental conditions. In this study, a strain of <i>Lactobacillus plantarum</i> SDJ09 with strong biofilm formation properties was screened from our laboratory collection of LAB, and then the AI-2 signaling inhibitor D-galactose was employed as a targeted intervention tool to dissect the role of Autoinducer-2 (AI-2) in biofilm regulation. Using this approach, the correlation between biofilm formation and AI-2 signaling was comprehensively investigated. With the help of metabolomics analyses, it was shown that D-galactoser could effectively affect biofilm formation by regulating the properties of biofilm components with inhibiting the transcriptional levels of amino acids, purines and eDNA. Meanwhile, real-time fluorescence quantitative PCR (RT-qPCR) was also performed to further analyze AI-2-related genes. It was found that D-galactoser could significantly reduce the expression of key genes, including the QS transcriptional regulator <i>LsrR</i> and exopolysaccharide synthesis genes (<i>LamA</i>, <i>LamC</i>), while leaving the AI-2 synthase gene <i>LuxS</i> largely unaffected. Collectively, it was indicated that the regulation of biofilm formation in <i>L. plantarum</i> SDJ09 by the <i>LuxS</i>/AI-2 QS system involved the modulation of downstream gene expression and metabolic pathways. The AI-2 signaling inhibitor D-galactose could disrupt this regulatory process, likely by impairing AI-2-mediated signal transduction, which subsequently suppressed biofilm development. These findings provided insights into the QS-based regulatory network of biofilm formation in probiotic lactobacilli and suggested that targeting AI-2 signaling could represent a strategy for modulating biofilm assembly.</p>

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The mechanism of LuxS/AI-2 QS system regulating the biofilm formation of Lactobacillus plantarum SDJ09

  • 期刊论文

  • 发表日期：

    2026年3月28日

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  • Mengyu Liu,
  • Xiaochun Su,
  • Ting Ma,
  • Lijia Liu,
  • Jiamin Xu,
  • Xiaoling Liu,
  • Yunxia Bai,
  • Shubo Li,
  • Yuan Guo

摘要

Lactic acid bacteria (LAB) have anti-inflammatory, hypolipidemic and hypoglycemic properties, as well as the ability to maintain intestinal flora balance, but are susceptible to inactivation by environmental stresses. To solve the above issues, improving biofilm formation has been applied to enhance bacterial resistance to environmental conditions. In this study, a strain of Lactobacillus plantarum SDJ09 with strong biofilm formation properties was screened from our laboratory collection of LAB, and then the AI-2 signaling inhibitor D-galactose was employed as a targeted intervention tool to dissect the role of Autoinducer-2 (AI-2) in biofilm regulation. Using this approach, the correlation between biofilm formation and AI-2 signaling was comprehensively investigated. With the help of metabolomics analyses, it was shown that D-galactoser could effectively affect biofilm formation by regulating the properties of biofilm components with inhibiting the transcriptional levels of amino acids, purines and eDNA. Meanwhile, real-time fluorescence quantitative PCR (RT-qPCR) was also performed to further analyze AI-2-related genes. It was found that D-galactoser could significantly reduce the expression of key genes, including the QS transcriptional regulator LsrR and exopolysaccharide synthesis genes (LamA, LamC), while leaving the AI-2 synthase gene LuxS largely unaffected. Collectively, it was indicated that the regulation of biofilm formation in L. plantarum SDJ09 by the LuxS/AI-2 QS system involved the modulation of downstream gene expression and metabolic pathways. The AI-2 signaling inhibitor D-galactose could disrupt this regulatory process, likely by impairing AI-2-mediated signal transduction, which subsequently suppressed biofilm development. These findings provided insights into the QS-based regulatory network of biofilm formation in probiotic lactobacilli and suggested that targeting AI-2 signaling could represent a strategy for modulating biofilm assembly.