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Unraveling the biofilm armor: How ROS drives biofilm formation in aquatic pathogen Edwardsiella piscicida

文献类型： 外文期刊

作者： Fang, Qingjian 1 ; Gou, Yin 2 ; Gu, Hanjie 2 ; Wu, Qingjuan 2 ; He, Jiaojiao 2 ; Li, Chenghua 1 ; Sun, Bin 4 ; Hu, Yonghua 2 ;

作者机构： 1.Ningbo Univ, Sch Marine Sci, Ningbo 315211, Peoples R China

2.Chinese Acad Trop Agr Sci, Inst Trop Biosci & Biotechnol, Sanya Res Inst, Sanya 572024, Peoples R China

3.Qingdao Marine Sci & Technol Ctr, Lab Marine Biol & Biotechnol, Qingdao, Peoples R China

4.Fujian Acad Agr Sci, Inst Biotechnol, Wusi Rd 247, Fuzhou 350003, Peoples R China

5.Hainan Prov Key Lab Funct Components Res & Utiliza, Haikou 571101, Peoples R China

关键词： Edwardsiella piscicida; Biofilm formation; Regulatory pathway; Oxidative stress; Virulence

期刊名称：AQUACULTURE （ 影响因子：3.9； 五年影响因子：4.4 ）

ISSN： 0044-8486

年卷期： 2025 年 609 卷

页码：

收录情况： SCI

摘要： Excessive reactive oxygen species (ROS) in the environment and within host cells present a serious threat to the survival and infectivity of pathogenic bacteria. Bacterial biofilm is recognized as a crucial resistance strategy against ROS. However, the mechanisms by which pathogenic bacteria respond to ROS to facilitate biofilm formation, particularly in aquatic pathogens, remain poorly understood. In our prior study, we generated a mutant (designated as ztrxAC) with elevated ROS levels by knocking out trxA and trxC of the thioredoxin system (Trx) in Edwardsiella piscicida, a ubiquitous pathogen causing serious economic losses in aquaculture. In this study, we observed that, compared to the wild type (WT), the biofilm growth and expression of cellulose biosynthesis genes in ztrxAC were significantly enhanced, while complementation strain of ztrxAC by expressing grx1 exhibited restored redox homeostasis and biofilm formation, indicating that elevated ROS promotes E. piscicida's capability of biofilm formation. We also observed a substantial increase in the levels of c-di-GMP, a vital signaling molecule involved in cellulose production and biofilm formation, in ztrxAC. The expression of phosphodiesterase YhjH, which degrades c-di-GMP, was decreased in ztrxAC and negatively correlated with biofilm formation. Consistently, ztrxAC exhibited a reduction in the expression of the regulatory factor FliA, which positively regulates the expression of yhjH. Regarding pathogenicity, the Trx mutation diminished the proliferation of E. piscicida in host cells and tissues, but it enhanced bacterial hemolytic activity, a virulence trait closely associated with biofilm formation, suggesting that the impact of ROS on bacterial virulence is multifaceted and intricate. In summary, this study elucidates for the first time the pathway through which E. piscicida responds to ROS to promote biofilm formation, as well as its implication for pathogenicity. These findings provide insights into the pathogenic mechanisms of E. piscicida and inform the development of novel strategies for preventing infections caused by this pathogen.

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