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LtrA对于副溶血性弧菌在食品相关表面形成生物膜和定殖至关重要。

LtrA is critical for biofilm formation and colonization of Vibrio parahaemolyticus on food-related surfaces.

作者信息

Xiong Shuhui, Zhang Nan, Sun Hui, Zhang Miaomiao, Li Xue, Luo Xi, Zhang Yiquan, Lu Renfei

机构信息

Department of Clinical Laboratory, Nantong Third People's Hospital, Affiliated Nantong Hospital 3 of Nantong University, Nantong 226006, Jiangsu, China; School of Medicine, Nantong University, Nantong 226001, Jiangsu, China.

Department of Clinical Laboratory, Nantong Third People's Hospital, Affiliated Nantong Hospital 3 of Nantong University, Nantong 226006, Jiangsu, China; School of Medicine, Jiangsu University, Zhenjiang 212013, Jiangsu, China.

出版信息

Int J Food Microbiol. 2025 Oct 2;441:111327. doi: 10.1016/j.ijfoodmicro.2025.111327. Epub 2025 Jun 24.

Abstract

Vibrio parahaemolyticus is the leading causative agent of seafood-associated acute gastroenteritis. The formation of biofilms is one of the key reasons for its resistance to adverse environments and its persistence in seafood. Investigating the regulatory mechanisms of biofilm formation is beneficial for the development of new intervention methods to reduce V. parahaemolyticus contamination during seafood processing and storage. In this study, we identified a global regulator, LtrA (VPA0519), which is involved in regulating biofilm formation in V. parahaemolyticus. The deletion of ltrA led to a significant alteration in the transcription levels of 706 genes, including those associated with type III and VI secretion systems and biofilm formation. LtrA positively regulated biofilm formation by enhancing the production of exopolysaccharides, extracellular proteins, extracellular DNA, and cyclic di-GMP (c-di-GMP), as well as by decreasing swimming and swarming motility. The deletion of the ltrA gene also led to a reduction in the metabolic activity of biofilm cells but did not affect the production of capsular polysaccharide. Furthermore, the deletion of the ltrA gene resulted in a decrease in the biofilm formation ability of V. parahaemolyticus on the surfaces of shrimp (Parapenaeopsis hardwickii), crab (Portunus trituberculatus), polypropylene plastic, glass, and stainless steel. The findings in this study extend our understanding of the roles of LtrA and the genetic determinants involved in biofilm formation by V. parahaemolyticus.

摘要

副溶血性弧菌是与海鲜相关的急性肠胃炎的主要致病原。生物膜的形成是其对恶劣环境具有抗性并能在海鲜中持续存在的关键原因之一。研究生物膜形成的调控机制有助于开发新的干预方法,以减少海鲜加工和储存过程中的副溶血性弧菌污染。在本研究中,我们鉴定出一种全局调节因子LtrA(VPA0519),它参与调控副溶血性弧菌的生物膜形成。ltrA基因的缺失导致706个基因的转录水平发生显著变化,包括那些与III型和VI型分泌系统以及生物膜形成相关的基因。LtrA通过增强胞外多糖、胞外蛋白、胞外DNA和环二鸟苷酸(c-di-GMP)的产生,以及降低游动和群游运动性,正向调控生物膜形成。ltrA基因的缺失还导致生物膜细胞的代谢活性降低,但不影响荚膜多糖的产生。此外,ltrA基因的缺失导致副溶血性弧菌在虾(哈氏仿对虾)、蟹(三疣梭子蟹)、聚丙烯塑料、玻璃和不锈钢表面的生物膜形成能力下降。本研究的结果扩展了我们对LtrA的作用以及副溶血性弧菌生物膜形成所涉及的遗传决定因素的理解。

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