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转录组分析揭示了Y0-C10-HSL对……生物膜形成和运动的作用机制 。 (注:原文中“of”后面似乎缺少具体内容)

Transcriptome Analysis Reveals the Mechanism of Y0-C10-HSL on Biofilm Formation and Motility of .

作者信息

Tang Deping, Liu Yali, Yao Huihui, Lin Yanyan, Xi Yanpeng, Li Mengjiao, Mao Aihong

机构信息

School of Biological & Pharmaceutical Engineering, Lanzhou Jiaotong University, Lanzhou 730070, China.

Gansu Provincial Academic Institute for Medical Research, Lanzhou 730050, China.

出版信息

Pharmaceuticals (Basel). 2024 Dec 19;17(12):1719. doi: 10.3390/ph17121719.

Abstract

() is a type of pathogen that takes advantage of opportunities to infect and form biofilm during infection. Inhibiting biofilm formation is a promising approach for the treatment of biofilm-related infections. Here, Y0-C10-HSL (N-cyclopentyl-n-decanamide) was designed, synthesized, and tested for its effect on biofilm formation, motility, and the () survival assay. In addition, the molecular mechanism of Y0-C10-HSL on biofilm formation was explored using transcriptome analysis. At a concentration of 200 μmol/L Y0-C10-HSL, biofilm and exopolysaccharides were decreased by 38.5% and 29.3%, respectively; Y0-C10-HSL effectively dispersed the pre-formed biofilm and inhibited the motility ability of ; and the survival assay showed that Y0-C10-HSL was safe and provided protection to against infection (the survival rates of were higher than 74% and increased by 39%, 35.1%, and 47.5%, respectively, when treated with 200 μmol/L Y0-C10-HSL at 24, 48, and 80 h). Transcriptome analysis showed that 585 differentially expressed genes (DEGs) were found after treatment with 200 μmol/L Y0-C10-HSL, including 254 up-regulated DEGs and 331 down-regulated DEGs. The genes involved in the quorum sensing system and biofilm formation were down-regulated. Y0-C10-HSL inhibited the biofilm formation and dispersed the pre-formed biofilm of through down-regulated genes related to quorum sensing pathways and biofilm formation. These findings provide a theoretical foundation for the treatment and prevention of antibiotic resistance in clinical and environmental microorganisms such as .

摘要

()是一种利用机会进行感染并在感染过程中形成生物膜的病原体。抑制生物膜形成是治疗与生物膜相关感染的一种有前景的方法。在此,设计、合成了Y0-C10-HSL(N-环戊基-n-癸酰胺),并测试了其对生物膜形成、运动性以及()存活试验的影响。此外,利用转录组分析探索了Y0-C10-HSL对生物膜形成的分子机制。在200μmol/L的Y0-C10-HSL浓度下,生物膜和胞外多糖分别减少了38.5%和29.3%;Y0-C10-HSL有效分散了预先形成的生物膜并抑制了()的运动能力;并且存活试验表明Y0-C10-HSL是安全的,并为()提供了针对()感染的保护(在24、48和80小时用200μmol/L Y0-C10-HSL处理时,()的存活率分别高于74%,并分别提高了39%、35.1%和47.5%)。转录组分析表明,用200μmol/L Y0-C10-HSL处理后发现了585个差异表达基因(DEG),包括254个上调的DEG和331个下调的DEG。参与群体感应系统和生物膜形成的基因被下调。Y0-C10-HSL通过下调与群体感应途径和生物膜形成相关的基因来抑制生物膜形成并分散预先形成的()生物膜。这些发现为治疗和预防临床和环境微生物如()中的抗生素耐药性提供了理论基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d6b/11678461/b35ee02bcb59/pharmaceuticals-17-01719-g001.jpg

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