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<p><i>Glaesserella parasuis</i> (<i>G. parasuis</i>), a lethal pathogen causing Glässer’s disease, poses severe threats to global swine health. While the small GTPase Ras homolog gene family member A (<i>RHOA</i>) is implicated in viral pathogenesis, its role in bacterial infections remains unexplored. Here, we established an in vitro infection model using porcine LLC-PK1 cells and demonstrated that <i>G. parasuis</i> induces adhesion and pseudopodia-mediated invasion, resulting in approximately 99% cell death within 120&#xa0;h post-infection. Crucially, <i>RHOA</i> expression was upregulated during infection, and <i>RHOA</i> knockout reduced bacterial adhesion and invasion, rescuing cell viability to 77.30%. Transcriptomic profiling of <i>RHOA</i>-knockout cells revealed 1797 differentially expressed genes, revealing indirect effects on cytoskeleton remodeling (<i>ACTG1</i>/<i>MYL7/MYL9</i> downregulation) and tight junction stabilization (<i>CDH1</i>/<i>CLDN1/CDH5</i> upregulation). This establishes <i>RHOA</i> as a key host factor facilitating <i>G. parasuis</i> infection, providing targets for disease control.</p>

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A novel function of RHOA as a host-dependent factor in Glaesserella parasuis infection of LLC-PK1 cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月25日

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  • Huanhuan Zhou,
  • Xuexue Chen,
  • Xinqi Zeng,
  • Shengsong Xie,
  • Xiaoyu Zhang,
  • Jiayi Zeng,
  • Ke Xu,
  • Bo Yu,
  • Hailong Liu,
  • Hongbo Chen

摘要

Glaesserella parasuis (G. parasuis), a lethal pathogen causing Glässer’s disease, poses severe threats to global swine health. While the small GTPase Ras homolog gene family member A (RHOA) is implicated in viral pathogenesis, its role in bacterial infections remains unexplored. Here, we established an in vitro infection model using porcine LLC-PK1 cells and demonstrated that G. parasuis induces adhesion and pseudopodia-mediated invasion, resulting in approximately 99% cell death within 120 h post-infection. Crucially, RHOA expression was upregulated during infection, and RHOA knockout reduced bacterial adhesion and invasion, rescuing cell viability to 77.30%. Transcriptomic profiling of RHOA-knockout cells revealed 1797 differentially expressed genes, revealing indirect effects on cytoskeleton remodeling (ACTG1/MYL7/MYL9 downregulation) and tight junction stabilization (CDH1/CLDN1/CDH5 upregulation). This establishes RHOA as a key host factor facilitating G. parasuis infection, providing targets for disease control.