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群体感应淬灭AHL-内酯酶Est816抑制多微生物龈下菌斑来源的生物膜形成。

Quorum-Quenching AHL-Lactonase Est816 Inhibits Polymicrobial Subgingival-Plaque-Derived Biofilm Formation.

作者信息

Zhao Zelda Ziyi, Shan Wenwen, Sun Xiaoyu, Cheng Tianfan, Zhang Jing, Chu Chun Hung

机构信息

Faculty of Dentistry, The University of Hong Kong, Hong Kong SAR, China.

Key Laboratory of Oral Diseases Research of Anhui Province, College & Hospital of Stomatology, Anhui Medical University, Hefei 230032, China.

出版信息

Dent J (Basel). 2025 Aug 15;13(8):372. doi: 10.3390/dj13080372.

Abstract

: This study aimed to investigate the effects of the quorum-quenching enzyme -acyl-homoserine lactone (AHL)-lactonase Est816 on biofilm formation in subgingival plaque microbiota from participants with advanced periodontitis. : Subgingival plaque samples were collected from 30 adults with untreated Stage III or higher periodontitis and cultured anaerobically. Est816 was applied in vitro, with phosphate-buffered saline (PBS) serving as the control. Biofilm composition was analyzed via 16S rRNA sequencing, and alpha diversity metrics were assessed. Differential taxa abundance was assessed with the multivariate statistical software MaAsLin3. Biofilm morphology, biomass, and thickness were evaluated using scanning electron microscopy (SEM), crystal violet staining, and confocal laser scanning microscopy (CLSM). : Est816 significantly reduced microbial richness (Chao1 Index, = 0.031), biofilm biomass (64% reduction, < 0.001), and thickness (76% reduction, < 0.001) compared to controls. SEM revealed fragmented biofilm architecture in Est816-treated samples. : AHL-lactonase Est816 inhibited polymicrobial subgingival-plaque-derived biofilm formation while reducing species richness, phylogenetic diversity, and community evenness. These findings demonstrate Est816's potential as an adjunctive therapy for disrupting pathogenic biofilms in periodontitis.

摘要

本研究旨在调查群体感应淬灭酶——酰基高丝氨酸内酯(AHL)-内酯酶Est816对晚期牙周炎患者龈下菌斑微生物群生物膜形成的影响。从30名未经治疗的III期或更严重牙周炎的成年人中采集龈下菌斑样本,并进行厌氧培养。在体外应用Est816,以磷酸盐缓冲盐水(PBS)作为对照。通过16S rRNA测序分析生物膜组成,并评估α多样性指标。使用多元统计软件MaAsLin3评估差异分类群丰度。使用扫描电子显微镜(SEM)、结晶紫染色和共聚焦激光扫描显微镜(CLSM)评估生物膜形态、生物量和厚度。与对照组相比,Est816显著降低了微生物丰富度(Chao1指数, = 0.031)、生物膜生物量(减少64%, < 0.001)和厚度(减少76%, < 0.001)。SEM显示Est816处理的样本中生物膜结构破碎。AHL-内酯酶Est816抑制了多微生物龈下菌斑来源的生物膜形成,同时降低了物种丰富度、系统发育多样性和群落均匀度。这些发现证明了Est816作为破坏牙周炎致病性生物膜的辅助治疗方法的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ed/12385154/df5c519444be/dentistry-13-00372-g001.jpg

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