<p><i>Klebsiella oxytoca</i> can cause gastrointestinal infections in humans. Within the instestinal tract, the bacterium encounters diverse host-derived signals (most notably bile salts, BS) and secondary metabolites (such as short-chain fatty acid salts, SCFAs) produced by microbial community. However, the mechanism of <i>K. oxytoca</i> response to BS and SCFAs stresses has been rarely reported. Recently, we found <i>K. oxytoca</i> in 14 species of aquatic food animals, of which <i>K. oxytoca</i> 7-7-27 of mussel origin had strong biofilm formation characteristics and many putative virulence-associated genes. Herein, we investigated the impact of normal physiological concentrations of BS (0.2% – 2.2%) and SCFAs (0.4% – 2.0%) in the tract on survival and virulence of <i>K. oxytoca</i> 7-7-27. The results revealed that the major BS (0.2% sodium cholate, or 0.8% sodium glycocholate) and SCFAs (0.4% sodium acetate, or 0.4% sodium butyrate) stimulated the bacterial growth, and significantly increased cell surface hydrophobicity, auto-aggregation rate and biofilm formation, as well as adhesion and invasion rates of <i>K. oxytoca</i> 7-7-27 toward the human colon Caco-2 cell (<i>p</i> &lt; 0.05). Notably, comparative secretomic and proteomic analyses uncovered a number of differentially secreted (i.e., 53) and produced (i.e., 1,049) proteins, as well as putative virulence-associated proteins (i.e., 69) triggered by the BS and SCFAs. <i>K. oxytoca</i> adopted multiple strategies to cope with the BS and SCFAs stresses. The results of this study highlighted the potential risk of ingestion of <i>K. oxytoca</i>-contaminated aquatic products.</p>

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Bile and short-chain fatty acid salts affect survival and virulence of Klebsiella Oxytoca of mussel origin

  • Jingjing Xu,
  • Meng Sun,
  • Jiangcheng Chang,
  • Qingchao Xie,
  • Yongjie Wang,
  • Lanming Chen

摘要

Klebsiella oxytoca can cause gastrointestinal infections in humans. Within the instestinal tract, the bacterium encounters diverse host-derived signals (most notably bile salts, BS) and secondary metabolites (such as short-chain fatty acid salts, SCFAs) produced by microbial community. However, the mechanism of K. oxytoca response to BS and SCFAs stresses has been rarely reported. Recently, we found K. oxytoca in 14 species of aquatic food animals, of which K. oxytoca 7-7-27 of mussel origin had strong biofilm formation characteristics and many putative virulence-associated genes. Herein, we investigated the impact of normal physiological concentrations of BS (0.2% – 2.2%) and SCFAs (0.4% – 2.0%) in the tract on survival and virulence of K. oxytoca 7-7-27. The results revealed that the major BS (0.2% sodium cholate, or 0.8% sodium glycocholate) and SCFAs (0.4% sodium acetate, or 0.4% sodium butyrate) stimulated the bacterial growth, and significantly increased cell surface hydrophobicity, auto-aggregation rate and biofilm formation, as well as adhesion and invasion rates of K. oxytoca 7-7-27 toward the human colon Caco-2 cell (p < 0.05). Notably, comparative secretomic and proteomic analyses uncovered a number of differentially secreted (i.e., 53) and produced (i.e., 1,049) proteins, as well as putative virulence-associated proteins (i.e., 69) triggered by the BS and SCFAs. K. oxytoca adopted multiple strategies to cope with the BS and SCFAs stresses. The results of this study highlighted the potential risk of ingestion of K. oxytoca-contaminated aquatic products.