变异链球菌密度感应系统调控变链素的研究进展

密度感应是指细菌根据菌群密度的变化分泌和感应信号分子一感受态调节肽(CSP),调控相关基因的表达.变链素是变异链球菌合成分泌的抗菌性多肽,在菌群中可调节相关细菌的生物学行为.变异链球菌密度感应系统可调控变链素的合成和分泌,参与菌群间的交流,调控牙菌斑生物膜的稳定性.下面就近年来受密度感应系统调控的变链素的研究进展作一综述.     

密度感应在口腔链球菌感染中的作用机制

口腔链球菌之间可以通过密度感应进行交流，分泌和感应特定的信号分子，从而感应周围环境群体细菌的密度，同时激活相关基因的表达，以协调菌群生物学行为。密度感应与口腔链球菌的生存和致病密切相关，其可能成为控制链球菌致病的有效途径。     

密度感应在口腔链球菌感染中的作用机制

口腔链球菌之间可以通过密度感应进行交流,分泌和感应特定的信号分子,从而感应周围环境群体细菌的密度,同时激活相关基因的表达,以协调菌群生物学行为。密度感应与口腔链球菌的生存和致病密切相关,其可能成为控制链球菌致病的有效途径。     

密度感应相关性变链素及其作用分析

细菌素是由某些细菌在代谢过程中产生的一类具有抗菌活性的蛋白质或多肽,变异链球菌产生的细菌素称为变链素.变链素可能与口腔生物膜中变异链球菌的致龋性及其在牙面的定植有关.目前已有多种变链素被分离、纯化并完成了基因序列和氨基酸序列的测定,变链素与密度感应调控系统的关系及在新型抗菌制剂研发中的应用价值已受到人们关注.本文就密度...     

变形链球菌ComCDE密度感应参与不同菌种的竞争

目的 研究口腔变形链球菌( S.mutans )ComCDE密度感应系统参与血链球菌(S.sanguinis)的相互竞争作用.方法 采用LIVE\DEAD BacLightTM荧光染色结合激光共聚焦显微镜,观察变形链球菌(简称变链菌)在CSP信号肽诱导下群体细菌自身死亡变化;通过荧光定量反转录聚合酶链反应(RT-PCR)测定细菌素以及细菌素免疫蛋白相关基因表达变化,分析变链菌ComCDE系统参与菌群生存竞争的调控机制.结果 在细菌竞争中,变形链球菌△comC、△comD 、△comE突变株失去不同菌种间的竞争力,无法抑制相邻Ssanguinis的正常生长;只有野生株保持竞争力,抑制相邻S.sanguinis生长,形成缺陷菌环.CSP信号肽诱导下,变链菌群体死菌/活菌率增高58.1％(P＜0.05);细菌素及免疫蛋白相关SMU.151、SMU.423、SMU.1913c基因分别升高23.3倍(P=0.00)、15.9倍(P＜0.05)、19.3倍(P＜0.05).结论 变形链球菌ComCDE密度感应系统调控变链菌的变链素及免疫蛋白产生、参与不同菌种间竞争生存.     

变异链球菌密度感应信号分子AI-2的研究进展

密度感应是细菌根据菌群密度的变化,分泌和感应特定的信号分子,激活相关基因的表达,从而调节细菌生物学行为的一种机制。目前细菌信号分子自体诱导物Ⅱ(autoinducer 2,AI-2)被认为是细菌通用的信号分子,参与口腔细菌间的交流,调控牙菌斑生物膜的稳定性。本文即对密度感应信号分子AI-2的合成转运及调控作用方面的研究进展作一综述。     

双组分信号传导系统与变异链球菌的致病相关特性

双组分信号传导系统(TCSTS)在变异链球菌感受态形成、生物膜形成、结构稳定、菌素产生、产酸耐酸特性等毒力因子表达方面起着重要的作用,为其在菌斑生物膜中的竞争和生存提供了诸多生态性优势.本文就变异链球菌TCSTS的组成、TCSTS对变异链球菌致病相关特性的影响、TCSTS的应用意义等作一综述.     

变形链球菌信号传导系统研究进展

变形链球菌通过信号传导系统来感应外界环境信号,改变相关基因的表达以适应环境因素的变化。本文介绍了信号传导系统的基本结构和作用机制,以及信号传导系统对变链菌生物学活性的调控作用,如介导感受态的产生、调控生物膜的形成等。探明信号传导系统在变链菌致病过程中的作用机制,可为控制变链菌感染提供另一种思路。     

变形链球菌LuxS蛋白与LuxS/AI-2群体感应系统的研究进展

口腔环境是一个多菌群共存的环境,变形链球菌是口腔主要致龋菌之一。群体感应使细菌能够感受自身和其他细菌的变化,适应环境,协调菌群之间的生存,已经成为新的药物干扰靶点。与变形链球菌群体感应密切相关的主要是LuxS蛋白和信号分子AI-2,本文从LuxS蛋白的基因、结构、作用机制和功能到LuxS/AI-2群体感应系统的作用作一综述。     

口腔变形链球菌感受态刺激因子的蛋白合成及活性检测

目的探讨口腔变形链球菌(S.mutans)密度感应系统信号蛋白的体外合成及其生物活性。方法采用化学合成法口腔S.mutans密度感应感受态刺激因子(CSP)信号蛋白,通过高效液相色谱仪纯化合成蛋白,质谱分析结构,通过扫描电镜对比观察CSP信号蛋白对S.mutans生物膜形成的影响,分析CSP信号蛋白的生物活性。结果化学合成纯化S.mutans CSP蛋白分子,加入CSP信号肽后,S.mutans生物膜呈团状密集分布,细菌之间存在厚实的黏性胞外分泌物,细菌黏连呈链团状。结论成功合成口腔S.mutans CSP信号蛋白,该蛋白肽具备促进S.mutans生物膜形成的生物活性。     

变形链球菌中LuxS介导的群体感应系统的研究进展

LuxS介导的群体感应系统以自体诱导物-2（AI-2）分子作为通用信号,可介导不同细菌的交流。作为口腔致龋生物膜中主要致病菌的变形链球菌中也存在这种感应系统。本文就LuxS信号系统在变形链球菌生物膜形成和毒力因子分泌方面的作用以及它所介导的变形链球菌与口腔中其他细菌的交流等内容作一综述。     

Quorum Sensing of Periodontal Pathogens

The term ‘quorum sensing’ describes intercellular bacterial communication which regulates bacterial gene expression according to population cell density. Bacteria produce and secrete small molecules, named autoinducers, into the intercellular space. The concentration of these molecules increases as a function of population cell density. Once the concentration of the stimulatory threshold is reached, alteration in gene expression occurs. Gram-positive and Gram-negative bacteria possess different types of quorum sensing systems. Canonical LuxI/R-type/acyl homoserine lactone mediated quorum sensing system is the best studied quorum sensing circuit and is described in Gram-negative bacteria which employ it for inter-species communication mostly. Gram-positive bacteria possess a peptide-mediated quorum sensing system. Bacteria can communicate within their own species (intra-species) but also between species (inter-species), for which they employ an autoinducer-2 quorum sensing system which is called the universal language of the bacteria. Periodontal pathogenic bacteria possess AI-2 quorum sensing systems. It is known that they use it for regulation of biofilm formation, iron uptake, stress response and virulence factor expression. A better understanding of bacterial communication mechanisms will allow the targeting of quorum sensing with quorum sensing inhibitors to prevent and control disease.Key Words: Quorum Sensing, Gram-Positive Bacteria, Gram-Negative Bacteria, Periodontitis     

群体感应系统对牙周致病菌影响的研究进展

牙周炎是人类最好发的口腔疾病之一,牙菌斑细菌作为牙周炎的始动因子,是导致牙周炎的首要因素。群体感应系统依靠群体感应信号分子调节不同种类细菌之间的通信,加强细菌之间的交流,促进疾病的发生发展。群体感应系统亦对牙菌斑细菌形成生物膜起到重要的促进作用。近年来,许多研究表明群体感应抑制剂可以有效减弱细菌间的群体感应并抑制和降低细菌生物膜的形成和毒力因子的表达。该文就群体感应系统对牙周炎致病菌影响的研究进展进行综述。     

Estimation of salivary bacteria capable of inhibiting and stimulating Streptococcus mutans and its correlation to dental caries and untreated carious teeth

Bacteriocins are bacteriocidal proteinaceous molecules produced by the Gram-positive bacteria not active against the produced strain. Many investigations have revealed that certain bacteria using antibacterial or the inhibitory substance inhibit some other bacteria. A study was conducted in a group of 60 children to ascertain whether any correlation exists between the proportion of salivary bacteria inhibiting and stimulating Streptococcus mutans and the oral health indices (DMFT, deft and Community Periodontal Index of Treatment Needs). A definite inverse correlation was observed between the percentage of salivary inhibiting S. mutans and untreated carious teeth (UCT).     

呋喃C-30对变异链球菌生物膜早期形成的影响

目的：探讨密度感应拮抗剂呋喃C-30对变异链球菌生物膜早期形成的影响。方法：将体外合成的密度感应拮抗剂呋喃C-30按终浓度10、100μmol/L分别配制于含变异链球菌的牛心脑浸液培养基,37℃微需氧培养24h,形成生物膜后,用生物膜定量分析仪检测生物膜形成的量。结果：100μmol/L呋喃C-30组变异链球菌生物膜的形成受到显著抑制,磁珠成像开始减弱和完全消失的时间均迟于对照组;生物膜开始形成后,其生物膜形成指数低于对照组,差异有统计学意义（P〈0.05）。结论：呋喃C-30在100μmol/L浓度时能有效抑制变异链球菌生物膜的形成,其应用可能为龋病防治提供新的思路。     

Nuclear dot protein 52, an autophagy-associated protein,regulates Toll-like receptor signaling

Toll-like receptors (TLRs) recognize molecular patterns on various microbes and serve as innate immune sensors. After cognate ligand recognition, TLRs activate signaling pathways to induce innate immune defense mechanisms, which eliminate pathogenic microbes, including periodontogenic bacteria, to a certain extent. Recent findings have shown that TLR signaling is linked to induction of autophagy to facilitate direct killing of cytosol-invading bacteria within infected cells. However, whether autophagy has any regulatory effects on TLR signaling remains unclear. Our recent study showed that the signaling molecules Toll/interleukin-1 receptor homology domain-containing adaptor inducing interferon-β and tumor necrosis factor receptor-associated factor 6 are selectively degraded by autophagy after activation of TLR signal transduction. We found that the nuclear dot protein 52 (NDP52), an autophagy-associated protein, is involved in such degradation, negatively regulating TLR signaling. However, interestingly, this activity of NDP52 is strictly restricted by the deubiquitinase A20. Here, we describe an autophagy-associated regulatory function of NDP52 in TLR signaling on the basis of our recent findings.     

Selective modulation of bacterial attachment to oral epithelial cells by enzyme activities associated with poor oral hygiene

The present investigation explored the hypothesis that elevated levels of certain enzymes in the gingival crevicular environment of individuals with poor oral hygiene and/or gingival inflammation may modify the surfaces of epithelial cells and thereby modulate the types of bacteria which attach and colonize. Buccal epithelial cells treated with neuraminidase and certain proteases were used as a model for study. Bacteria studied included Streptococcus sanguis and Streptococcus mitis which have been associated with gingival health, Actinomyces species which are increased in plaque associated with developing gingivitis, and Bacteroides gingivalis, Bacteroides intermedius, and Actinobacillus actinomycetemcomitans which are associated with destructive periodontal diseases. Treatment of epithelial cells with the enzymes studied produced selective effects on their receptivity for bacteria. Neuraminidase treatment of epithelial cells greatly reduced the attachment of all strains of S. sanguis and S. mitis studied. In contrast, the number of Actinomyces viscosus, A. naeslundii and A. israelii cells which attached was significantly increased. Neuraminidase treatment also appeared to enhance attachment of B. intermedius and B. gingivalis. Treatment of buccal cells with trypsin, chymotrypsin or papain also selectively affected bacterial attachment. Such protease treatment greatly reduced the numbers of streptococci and A. viscosus cells which attached, while the numbers of B. gingivalis and B. intermedius were significantly increased. Treatment of epithelial cells with preparations of lysosomal enzymes derived from human PMNs produced similar selective effects. The changes in bacterial adhesion observed by the enzyme treatments studied are consistent with the shifts in the composition of the gingival crevice flora which occur when oral hygiene is terminated and gingivitis develops.     

茸毛链球菌对四种烤瓷合金腐蚀行为的影响

目的:研究口腔茸毛链球菌对4种烤瓷合金腐蚀性的影响,并探讨其影响是否因细菌作用环境不同而存在变化。方法:将受试合金与茸毛链球菌在固体或液体培养基中共同培养,以单纯培养基和空白组作为对照,10周后,用电化学方法对测试材料行动电位极化扫描,Corrview2腐蚀分析软件分析获得材料Icorr、Ecorr和Etp,并以场发射扫描电镜观察腐蚀后合金表面形貌。结果:电化学测试结果显示,细菌作用组(C组和D组)较无细菌作用组(B组)自腐蚀电位值偏负,且各合金液体培养基作用组(C组)较固体培养基组(D组)更负。SEM观察到合金表面孔蚀点。而无细菌作用的单纯培养基作用组(B组)较空白组(A组)自腐蚀电位值偏正。结论:口腔茸毛链球菌能够增加烤瓷合金的腐蚀倾向,使合金更易发生腐蚀;且口腔细菌在液体环境较固体环境对合金耐蚀性影响更大。