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变形链球菌来源的葡糖基转移酶的生物学特性:在致龋生物膜细胞外基质形成中的作用。

Biology of Streptococcus mutans-derived glucosyltransferases: role in extracellular matrix formation of cariogenic biofilms.

机构信息

Center for Oral Biology, University of Rochester, Rochester, NY 14642, USA.

出版信息

Caries Res. 2011;45(1):69-86. doi: 10.1159/000324598. Epub 2011 Feb 23.

Abstract

The importance of Streptococcus mutans in the etiology and pathogenesis of dental caries is certainly controversial, in part because excessive attention is paid to the numbers of S. mutans and acid production while the matrix within dental plaque has been neglected. S. mutans does not always dominate within plaque; many organisms are equally acidogenic and aciduric. It is also recognized that glucosyltransferases from S. mutans (Gtfs) play critical roles in the development of virulent dental plaque. Gtfs adsorb to enamel synthesizing glucans in situ, providing sites for avid colonization by microorganisms and an insoluble matrix for plaque. Gtfs also adsorb to surfaces of other oral microorganisms converting them to glucan producers. S. mutans expresses 3 genetically distinct Gtfs; each appears to play a different but overlapping role in the formation of virulent plaque. GtfC is adsorbed to enamel within pellicle whereas GtfB binds avidly to bacteria promoting tight cell clustering, and enhancing cohesion of plaque. GtfD forms a soluble, readily metabolizable polysaccharide and acts as a primer for GtfB. The behavior of soluble Gtfs does not mirror that observed with surface-adsorbed enzymes. Furthermore, the structure of polysaccharide matrix changes over time as a result of the action of mutanases and dextranases within plaque. Gtfs at distinct loci offer chemotherapeutic targets to prevent caries. Nevertheless, agents that inhibit Gtfs in solution frequently have a reduced or no effect on adsorbed enzymes. Clearly, conformational changes and reactions of Gtfs on surfaces are complex and modulate the pathogenesis of dental caries in situ, deserving further investigation.

摘要

变形链球菌在龋齿病因和发病机制中的重要性肯定是有争议的,部分原因是过度关注变形链球菌的数量和产酸,而忽视了牙菌斑中的基质。变形链球菌并不总是在菌斑中占主导地位;许多生物同样具有产酸和耐酸能力。人们还认识到,变形链球菌的葡糖基转移酶(Gtfs)在致龋性牙菌斑的发展中起着关键作用。Gtfs 吸附到釉质原位合成的葡聚糖上,为微生物的强烈定植提供了位点,并为菌斑提供了不溶性基质。Gtfs 还吸附到其他口腔微生物的表面,将其转化为葡聚糖生产者。变形链球菌表达 3 种遗传上不同的 Gtfs;每一种似乎在致龋性菌斑的形成中都发挥着不同但重叠的作用。GtfC 被吸附到菌膜中的釉质上,而 GtfB 则强烈结合细菌,促进紧密的细胞聚集,并增强菌斑的内聚性。GtfD 形成一种可溶性、易代谢的多糖,并作为 GtfB 的引物。可溶性 Gtfs 的行为与观察到的表面吸附酶不同。此外,由于菌斑内的突变酶和葡聚糖酶的作用,多糖基质的结构随时间而变化。不同部位的 Gtfs 为预防龋齿提供了化学治疗靶点。然而,抑制溶液中 Gtfs 的药物经常对吸附酶的抑制作用降低或没有作用。显然,Gtfs 在表面的构象变化和反应非常复杂,调节了原位龋齿的发病机制,值得进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba52/3068567/808766a1daa1/cre0045-0069-f01.jpg

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