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<p><i>Acinetobacter baumannii</i> is a formidable nosocomial pathogen whose multidrug resistance and immune evasion capabilities present a major therapeutic challenge. This study identifies the type VI secretion system (T6SS) effector VgrG2 as a critical virulence regulator in <i>A. baumannii</i>. VgrG2 employs a two-pronged strategy to undermine host innate immunity. First, it transcriptionally represses the major adhesin Csu pilus, reducing bacterial recognition, phagocytic uptake, and neutrophils recruitment. Second, VgrG2 directly targets and hyperactivates the small GTPase Rac1 within phagocytes. This leads to actin cytoskeletal disarray, which drives excessive macropinocytosis, resulting in compromised phagocytosis and methuosis—a non-apoptotic, vacuole-dependent death specific to phagocytes. Thus, VgrG2 selectively eliminates key immune sentinels and alters pulmonary inflammation, promoting bacterial persistence and dissemination. These findings extend the role of T6SS effectors beyond interbacterial competition to include sophisticated eukaryotic-directed attacks, and highlight the VgrG2-Rac1 axis as a promising therapeutic target.</p>

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The VgrG2 effector of Acinetobacter baumannii mediates immune evasion by repressing Csu pilus assembly and triggering phagocyte methuosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月27日

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  • Wenzeng Xu,
  • Jiancang Zhou,
  • Wang Zhang,
  • Yan Jiang,
  • Qingye Xu,
  • Xiaochen Liu,
  • Yisha Zhang,
  • Xiaoxiang Tan,
  • Junxin Zhou,
  • Luyun Cui,
  • Yake Yao,
  • Liang Liang,
  • Chengying Xu,
  • Xiaoting Hua,
  • Yunsong Yu,
  • Hua Zhou

摘要

Acinetobacter baumannii is a formidable nosocomial pathogen whose multidrug resistance and immune evasion capabilities present a major therapeutic challenge. This study identifies the type VI secretion system (T6SS) effector VgrG2 as a critical virulence regulator in A. baumannii. VgrG2 employs a two-pronged strategy to undermine host innate immunity. First, it transcriptionally represses the major adhesin Csu pilus, reducing bacterial recognition, phagocytic uptake, and neutrophils recruitment. Second, VgrG2 directly targets and hyperactivates the small GTPase Rac1 within phagocytes. This leads to actin cytoskeletal disarray, which drives excessive macropinocytosis, resulting in compromised phagocytosis and methuosis—a non-apoptotic, vacuole-dependent death specific to phagocytes. Thus, VgrG2 selectively eliminates key immune sentinels and alters pulmonary inflammation, promoting bacterial persistence and dissemination. These findings extend the role of T6SS effectors beyond interbacterial competition to include sophisticated eukaryotic-directed attacks, and highlight the VgrG2-Rac1 axis as a promising therapeutic target.