Exopolysaccharide from Lactobacillus casei NA-2 attenuates Escherichia coli O157:H7 surface adhesion via modulation of membrane surface properties and adhesion-related gene expression

文献类型： 外文期刊

第一作者： Ma, Lan

作者： Ma, Lan;Xu, Xiaoqing;Peng, Qing;Yang, Shuo;Zhang, Yuwei;Tian, Dandan;Shi, Linbo;Qiao, Yu;Shi, Bo

作者机构：

关键词： Exopolysaccharide; Escherichia coli; Bacterial adhesion; Surface properties; Biofilm

期刊名称：MICROBIAL PATHOGENESIS （ 影响因子：3.8； 五年影响因子：4.0 ）

ISSN： 0882-4010

年卷期： 2022 年 173 卷

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收录情况： SCI

摘要： The natural compound, exopolysaccharide from Lactobacillus casei NA-2 (EPS-cn2), has been shown to inhibit biofilm formation by Escherichia coli O157:H7. Although bacterial adhesion to substrate surfaces is a primary, indispensable step in this process, the mechanisms by which EPS-cn2 can block E. coli O157:H7 adhesion to biotic or abiotic surfaces remain unclear. In this study, investigation of E. coli O157:H7 response to EPS-cn2 revealed that 1 mg/mL EPS-cn2 can decrease adherence to polystyrene and confluent Caco-2 cell surfaces to 49.0% (P< 0.0001) and 57.0% (P<0.01) of that in untreated E. coli O157:H7, respectively. Moreover, EPS-cn2 significantly reduced outer membrane hydrophobicity by 49.0% and decreased the electronegativity of the membrane surface charge by as much as 1.57 mV (P<0.05) compared to untreated cells. High throughput RNA sequencing indicated that genes responsible for adhesion through extracellular matrix secretion, such as poly-N-acetylglucosamine (PNAG) biosynthesis, locus of enterocyte effacement (LEE) proteins and outer membrane protein (OmpT) were all down-regulated in response to EPS-cn2, while chemotaxis and motility-related flagellar assembly genes were differentially up-regulated, suggesting that the EPS-cn2 may serve as an extracellular signal to attenuate adhesion-related gene expression and alter bacterial surface properties in E. coli O157:H7. These findings support the further development of EPS-cn2 for pathogenic biofilm management in clinical and industrial settings, and suggests the further targeting of adhesion-related genes to limit the persistence of this highly pathogenic strain in sensitive environments.

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