N-acyl homoserine lactones lactonase est816 suppresses biofilm formation and periodontitis in rats mediated by Aggregatibacter actinomycetemcomitans.

IF 3.7 2区 医学 Q2 MICROBIOLOGY Journal of Oral Microbiology Pub Date : 2024-01-07 eCollection Date: 2024-01-01 DOI:10.1080/20002297.2023.2301200
Zelda Ziyi Zhao, Junmin Wang, Xinpai Liu, Zezhi Wang, Xianyu Zheng, Wuli Li, Tianfan Cheng, Jing Zhang
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Abstract

Aims: The current study aimed to explore the adjuvant therapeutic effect of N-acyl homoserine lactones (AHLs)-lactonase est816 on Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) biological behaviors and periodontitis progression.

Methods: The inhibitory properties of est816 were detected by live/dead bacterial staining, scanning electron microscope (SEM), crystal-violet staining and reverse-transcription quantitative PCR (RT-qPCR). Biocompatibility of est816 on human gingival fibroblasts (HGFs) and human gingival epithelial cells (HGEs) was evaluated by CCK8 and ELISA. The ligature-induced periodontitis model was established in rats. Micro computed tomography and immunohistochemical and histological staining served to evaluate the effect of est816 on the prevention of periodontitis in vivo.

Results: est816 significantly attenuated biofilm formation, reduced the mRNA expression of cytolethal distending toxin, leukotoxin and poly-N-acetyl glucosamine (PNAG) and downregulated expressions of interleukin-6 and tumor necrosis factor-α with low cell toxicity. In vivo investigations revealed est816 decreased alveolar bone resorption, suppressed matrix metalloproteinase-9 expression and increased osteoprotegerin expression.

Conclusion: est816 inhibited A. actinomycetemcomitans biofilm formation and virulence release, resulting in anti-inflammation and soothing of periodontitis in rats, indicating that est816 could be investigated in further research on periodontal diseases.

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N-acyl homoserine lactones lactonase est816 可抑制放线杆菌介导的大鼠生物膜形成和牙周炎。
目的:本研究旨在探讨N-酰基均丝氨酸内酯(AHLs)-内酯酶est816对放线菌属(A. actinomycetemcomitans)生物行为和牙周炎进展的辅助治疗作用:方法:通过活/死细菌染色、扫描电子显微镜(SEM)、水晶紫染色和反转录定量 PCR(RT-qPCR)检测 est816 的抑制特性。通过 CCK8 和 ELISA 评估了 est816 对人牙龈成纤维细胞(HGFs)和人牙龈上皮细胞(HGEs)的生物相容性。在大鼠身上建立了结扎诱导的牙周炎模型。结果表明:est816能显著减少生物膜的形成,降低细胞致死性膨胀毒素、白细胞毒素和聚-N-乙酰葡糖胺(PNAG)的mRNA表达,下调白细胞介素-6和肿瘤坏死因子-α的表达,且细胞毒性较低。结论:est816能抑制放线菌生物膜的形成和毒力释放,从而抗炎和舒缓大鼠牙周炎,表明est816可用于牙周疾病的进一步研究。
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来源期刊
CiteScore
8.00
自引率
4.40%
发文量
52
审稿时长
12 weeks
期刊介绍: As the first Open Access journal in its field, the Journal of Oral Microbiology aims to be an influential source of knowledge on the aetiological agents behind oral infectious diseases. The journal is an international forum for original research on all aspects of ''oral health''. Articles which seek to understand ''oral health'' through exploration of the pathogenesis, virulence, host-parasite interactions, and immunology of oral infections are of particular interest. However, the journal also welcomes work that addresses the global agenda of oral infectious diseases and articles that present new strategies for treatment and prevention or improvements to existing strategies. Topics: ''oral health'', microbiome, genomics, host-pathogen interactions, oral infections, aetiologic agents, pathogenesis, molecular microbiology systemic diseases, ecology/environmental microbiology, treatment, diagnostics, epidemiology, basic oral microbiology, and taxonomy/systematics. Article types: original articles, notes, review articles, mini-reviews and commentaries
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