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<p>Hypervirulent <i>Klebsiella pneumoniae </i>(hvKp), particularly sequence type 23 (ST23), is a predominant global cause of pyogenic liver abscesses. While ST23 hvKp is strongly associated with this invasive pathology, the molecular basis for its enhanced gut translocation potential, a critical prerequisite for hematogenous dissemination to the liver, remains unclear. Phylogenetic analysis of type 1 fimbrial gene clusters revealed that ST23 isolates uniquely encode a distinct combination of fimbrial subunits. Using engineered strains, we demonstrated that ST23-derived type 1 fimbriae, but not those from the ST11 lineage of classical <i>K. pneumoniae</i>, specifically bind to host enterocyte α3β1 integrins. This specific interaction conferred superior invasion capacity across intestinal epithelial barriers to ST23 hvKp compared to strains expressing ST11 fimbriae (<i>P</i> &lt; 0.05). Thus, ST23 hvKp exploits lineage-specific type 1 fimbriae to target α3β1 integrin, driving efficient gut epithelial invasion—a pivotal initial step in systemic dissemination leading to liver abscess formation. This work identifies a dedicated molecular invasion system intrinsic to ST23 hvKp, mechanistically explaining its enhanced invasive capacity and strong clinical association with pyogenic liver abscesses.</p>

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Lineage-specific type 1 fimbriae in hypervirulent ST23 Klebsiella pneumoniae target α3β1 integrin to promote intestinal epithelial invasion

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月23日

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  • Qian Zeng,
  • Ying Zhang,
  • Shujing Li,
  • Xinyue Fan,
  • Su Wang,
  • Jiayuan Liu,
  • Cui Tai,
  • Meng Li,
  • Yuanyuan Wei,
  • Yunkun Huang,
  • Yi Li,
  • Lefu Lan,
  • Xiaofei Jiang

摘要

Hypervirulent Klebsiella pneumoniae (hvKp), particularly sequence type 23 (ST23), is a predominant global cause of pyogenic liver abscesses. While ST23 hvKp is strongly associated with this invasive pathology, the molecular basis for its enhanced gut translocation potential, a critical prerequisite for hematogenous dissemination to the liver, remains unclear. Phylogenetic analysis of type 1 fimbrial gene clusters revealed that ST23 isolates uniquely encode a distinct combination of fimbrial subunits. Using engineered strains, we demonstrated that ST23-derived type 1 fimbriae, but not those from the ST11 lineage of classical K. pneumoniae, specifically bind to host enterocyte α3β1 integrins. This specific interaction conferred superior invasion capacity across intestinal epithelial barriers to ST23 hvKp compared to strains expressing ST11 fimbriae (P < 0.05). Thus, ST23 hvKp exploits lineage-specific type 1 fimbriae to target α3β1 integrin, driving efficient gut epithelial invasion—a pivotal initial step in systemic dissemination leading to liver abscess formation. This work identifies a dedicated molecular invasion system intrinsic to ST23 hvKp, mechanistically explaining its enhanced invasive capacity and strong clinical association with pyogenic liver abscesses.