Exopolysaccharides metabolism and cariogenesis of Streptococcus mutans biofilm regulated by antisense vicK RNA.

IF 3.7 2区 医学 Q2 MICROBIOLOGY
Yuting Sun, Hong Chen, Mengmeng Xu, Liwen He, Hongchen Mao, Shiyao Yang, Xin Qiao, Deqin Yang
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引用次数: 1

Abstract

Background: Streptococcus mutans (S. mutans) is a pivotal cariogenic pathogen contributing to its multiple virulence factors, one of which is synthesizing exopolysaccharides (EPS). VicK, a sensor histidine kinase, plays a major role in regulating genes associated with EPS synthesis and adhesion. Here we first identified an antisense vicK RNA (ASvicK) bound with vicK into double-stranded RNA (dsRNA).

Objective: This study aims to investigate the effect and mechanism of ASvicK in the EPS metabolism and cariogenesis of S. mutans.

Methods: The phenotypes of biofilm were detected by scanning electron microscopy (SEM), gas chromatography-mass spectrometery (GC-MS) , gel permeation chromatography (GPC) , transcriptome analysis and Western blot. Co-immunoprecipitation (Co-ip) assay and enzyme activity experiment were adopted to investigate the mechanism of ASvicK regulation. Caries animal models were developed to study the relationship between ASvicK and cariogenicity of S. mutans.

Results: Overexpression of ASvicK can inhibit the growth of biofilm, reduce the production of EPS and alter genes and protein related to EPS metabolism. ASvicK can adsorb RNase III to regulate vicK and affect the cariogenicity of S. mutans.

Conclusions: ASvicK regulates vicK at the transcriptional and post-transcriptional levels, effectively inhibits EPS synthesis and biofilm formation and reduces its cariogenicity in vivo.

Abstract Image

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反义vicK RNA调控变形链球菌生物膜外多糖代谢与龋齿发生。
背景:变形链球菌(S. mutans)是一种关键的致龋病原体,具有多种毒力因子,其中之一是合成外多糖(EPS)。VicK是一种传感器组氨酸激酶,在调节EPS合成和粘附相关基因中起主要作用。在这里,我们首先鉴定了一种反义的vicK RNA (ASvicK)与vicK结合成双链RNA (dsRNA)。目的:探讨ASvicK在变形链球菌EPS代谢和龋齿发生中的作用及其机制。方法:采用扫描电镜(SEM)、气相色谱-质谱(GC-MS)、凝胶渗透色谱(GPC)、转录组分析和Western blot检测生物膜的表型。采用共免疫沉淀法(Co-ip)和酶活性实验研究ASvicK的调控机制。为了研究ASvicK与变形链球菌致龋性的关系,建立了龋动物模型。结果:ASvicK过表达可以抑制生物膜的生长,减少EPS的产生,改变EPS代谢相关的基因和蛋白。ASvicK可以吸附RNase III调控vicK,影响变形链球菌的致癌性。结论:ASvicK在转录和转录后水平调控vicK,有效抑制EPS合成和生物膜形成,降低其体内致癌性。
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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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