Amonabactin Synthetase G Regulates Aeromonas hydrophila Pathogenicity Through Modulation of Host Wnt/β-catenin Signaling

作者：Yiyang Tang, Xiaofeng Liu, Chuyi Zeng, Yujun Liu, Ye Yang, Jiayi Hu, Pingyuan Li, Zejun Zhou · 发表于：Vaccines · 年份：2025 · DOI：10.3390/vaccines13020195 · 被引用次数：3 · 研究领域：Aquaculture disease management and microbiota、Vibrio bacteria research studies、Microbial infections and disease research

Background/Objectives: Aeromonas hydrophila is a significant opportunistic pathogen with a broad host range. It produces a catecholate siderophore, amonabactin, during iron starvation, but the in vivo infection mechanism that involves amonabactin is unclear. This study aims to elucidate the role of amonabactin synthetase G (AmoG) in the pathogenicity of A. hydrophila and its impact on gut barrier function. Methods: ΔAmoG was generated by deleting the AMP-binding domain of AmoG in A. hydrophila CCL1. In vivo infection experiments were conducted to assess the mutant’s iron-chelating ability and pathogenicity. Complementation of ΔAmoG with AmoG (ΔAmoG-C) was performed to confirm the observed phenotypes. Transcriptomic and qRT-PCR analyses were used to investigate gene expression changes in infected fish. Goblet cell counts, tight junction expression, and D-lactic acid and LPS levels were measured to evaluate gut barrier function. Results: ΔAmoG exhibited impaired iron-chelating ability and reduced pathogenicity compared to wild-type CCL1. Complementation with AmoG restored virulence in ΔAmoG-C. Transcriptomic and qRT-PCR analyses revealed an elevated expression of Wnt/β-catenin pathway components and antimicrobial genes in ΔAmoG-infected fish. Further investigation indicated increased goblet cells and an enhanced expression of tight junctions, as well as lower D-lactic acid and LPS levels, in ΔAmoG-infected fish. However, gut permeability, bacterial load, and lethality did not s...