Suppr超能文献

变形链球菌的 vicK 基因通过胞外多糖代谢介导其致龋性。

The vicK gene of Streptococcus mutans mediates its cariogenicity via exopolysaccharides metabolism.

机构信息

State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Department of Preventive Dentistry, West China Hospital of Stomatology, Sichuan University, 610041, Chengdu, China.

出版信息

Int J Oral Sci. 2021 Dec 16;13(1):45. doi: 10.1038/s41368-021-00149-x.

Abstract

Streptococcus mutans (S. mutans) is generally regarded as a major contributor to dental caries because of its ability to synthesize extracellular polysaccharides (EPS) that aid in the formation of plaque biofilm. The VicRKX system of S. mutans plays an important role in biofilm formation. The aim of this study was to investigate the effects of vicK gene on specific characteristics of EPS in S. mutans biofilm. We constructed single-species biofilms formed by different mutants of vicK gene. Production and distribution of EPS were detected through atomic force microscopy, scanning electron microscopy and confocal laser scanning microscopy. Microcosmic structures of EPS were analyzed by gel permeation chromatography and gas chromatography-mass spectrometry. Cariogenicity of the vicK mutant was assessed in a specific pathogen-free rat model. Transcriptional levels of cariogenicity-associated genes were confirmed by quantitative real-time polymerase chain reaction. The results showed that deletion of vicK gene suppressed biofilm formation as well as EPS production, and EPS were synthesized mostly around the cells. Molecular weight and monosaccharide components underwent evident alterations. Biofilms formed in vivo were sparse and contributed a decreased degree of caries. Moreover, expressional levels of genes related to EPS synthesis were down-regulated, except for gtfB. Our report demonstrates that vicK gene enhances biofilm formation and subsequent caries development. And this may due to its regulations on EPS metabolism, like synthesis or microcosmic features of EPS. This study suggests that vicK gene and EPS can be considered as promising targets to modulate dental caries.

摘要

变形链球菌(S. mutans)通常被认为是导致龋齿的主要原因,因为它能够合成有助于菌斑生物膜形成的细胞外多糖(EPS)。S. mutans 的 VicRKX 系统在生物膜形成中起着重要作用。本研究旨在研究 vicK 基因对 S. mutans 生物膜中 EPS 特定特性的影响。我们构建了由不同 vicK 基因突变体形成的单种生物膜。通过原子力显微镜、扫描电子显微镜和共聚焦激光扫描显微镜检测 EPS 的产生和分布。通过凝胶渗透色谱和气相色谱-质谱分析 EPS 的微观结构。在无特定病原体大鼠模型中评估 vicK 突变体的致龋性。通过定量实时聚合酶链反应证实与致龋性相关基因的转录水平。结果表明,vicK 基因缺失抑制了生物膜形成和 EPS 产生,并且 EPS 主要在细胞周围合成。分子量和单糖成分发生明显改变。体内形成的生物膜稀疏,导致龋齿程度降低。此外,与 EPS 合成相关的基因表达水平下调,除了 gtfB。我们的报告表明,vicK 基因增强了生物膜形成和随后的龋齿发展。这可能是由于其对 EPS 代谢的调节,如 EPS 的合成或微观特征。本研究表明,vicK 基因和 EPS 可以被视为调节龋齿的有前途的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa1/8677823/1a6ebe81ac0b/41368_2021_149_Fig1_HTML.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验