Salivary Film Expresses a Complex, Macromolecular Binding Site for Streptococcus sanguis

Gong, Ke; Mailloux, Lynn; Herzberg, Mark C.

doi:10.1074/jbc.275.12.8970

Cited by 44 publications

(29 citation statements)

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“…The pellicle on tooth enamel and restorative materials is formed by a selective adsorption of salivary macromolecules. In this light, the physicochemical properties of a material influences microbial adhesion either directly or through adsorption of salivary proteins 19,20) .…”

Section: Discussionmentioning

confidence: 99%

Adhesion of Streptococcus sanguinis to Dental Implant and Restorative Materials in vitro

et al. 2007

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Bacterial adhesion to tooth surfaces or dental materials starts immediately upon exposure to the oral environment. The aim of this study, therefore, was to compare the adhesion of Streptococcus sanguinis to saliva-coated human enamel and dental materials -during a one-hour period -using an in vitro flow chamber system which mimicked the oral cavity. After fluorescent staining, the number of adhered cells and their vitality were recorded. The dental materials used were: titanium (Rematitan M), gold (Neocast 3), ceramic (Vita Omega 900), and composite (Tetric Ceram).The number of adherent bacterial cells was higher on titanium, gold, and ceramic surfaces and lower on composite as compared to enamel. As for the percentage of adherent vital cells, it was higher on enamel than on the restorative materials tested. These results suggested that variations in the number and vitality of the adherent pioneer oral bacteria, S. sanguinis, in the in vitro system depended on the surface characteristics of the substratum and the acquired salivary pellicle.The in vitro adhesion model used herein provided a simple and reproducible approach to investigate the impact of surface-modified dental materials on bacterial adhesion and vitality.

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Section: Discussionmentioning

confidence: 99%

Adhesion of Streptococcus sanguinis to Dental Implant and Restorative Materials in vitro

et al. 2007

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“…The adhesion assay described by Gong et al (11) was modified to study biofilm formation by using the IVET library for S. gordonii. An overnight culture of the S. gordonii V288 reporter gene (amy-cat) fusion library in THB with TET was diluted 1,000-fold in FMC medium.…”

Section: Methodsmentioning

confidence: 99%

Involvement of Streptococcus gordonii Beta-Glucoside Metabolism Systems in Adhesion, Biofilm Formation, and In Vivo Gene Expression

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Lin

Zhang³

et al. 2004

J Bacteriol

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Streptococcus gordonii genes involved in beta-glucoside metabolism are induced in vivo on infected heart valves during experimental endocarditis and in vitro during biofilm formation on saliva-coated hydroxyapatite (sHA). To determine the roles of beta-glucoside metabolism systems in biofilm formation, the loci of these induced genes were analyzed. To confirm the function of genes in each locus, strains were constructed with gene inactivation, deletion, and/or reporter gene fusions. Four novel systems responsible for beta-glucoside metabolism were identified, including three phosphoenolpyruvate-dependent phosphotransferase systems (PTS) and a binding protein-dependent sugar uptake system for metabolizing multiple sugars, including beta-glucosides. Utilization of arbutin and esculin, aryl-beta-glucosides, was defective in some mutants. Esculin and oligochitosaccharides induced genes in one of the three beta-glucoside metabolism PTS and in four other genetic loci. Mutation of genes in any of the four systems affected in vitro adhesion to sHA, biofilm formation on plastic surfaces, and/or growth rate in liquid medium. Therefore, genes associated with beta-glucoside metabolism may regulate S. gordonii in vitro adhesion, biofilm formation, growth, and in vivo colonization.Streptococcus gordonii is a pioneer colonizer on the surface of human teeth, initiating the formation of dental plaque (25).Although not directly associated with dental or gingival diseases in the oral cavity, S. gordonii colonizes damaged heart valves once it enters the bloodstream in the experimental rabbit (15) and is considered to cause endocarditis in humans (1,8,12). Thus, the virulence of S. gordonii is reflected in its ability to adhere, colonize, and survive in the heart, where it is a pathogen, and on teeth in the oral cavity, where it is not. Its virulence in a specific environment may reflect expression of genes uniquely in that environment.Using an in vivo expression technology (IVET) library constructed in S. gordonii V288, at least 13 genes were shown to be expressed in vivo on infected heart valves during experimental endocarditis, but they were unexpressed in vitro under laboratory conditions (15). Since expression occurred only on heart valves, these genes were suggested to contribute to virulence and perhaps pathogenicity. Similarly, S. gordonii genes expressed during in vitro colonization of saliva-coated hydroxyapatite (sHA) were identified using the IVET library (17). Among the genes expressed during colonization of sHA and damaged heart valves in the rabbit were beta-glucoside metabolism-encoding genes. We therefore initiated in vitro studies to understand how the beta-glucoside metabolism genes might contribute to colonization of heart valves in infective endocarditis and on sHA.Bacteria ferment beta-glucoside sugar substrates, including cellobiose, arbutin, salicin, and esculin. While common in plants and useful in establishing phenotypic fermentation patterns of bacteria, the aryl-beta-disaccharides are not found in mammali...

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“…S. sanguinis binds directly to saliva-coated teeth, probably by a variety of mechanisms (46). Studies employing saliva-coated hydroxyapatite as a tooth model have revealed both lectin-carbohydrate and nonlectin interactions (27,38,42,64). Some of the salivary components to which S. sanguinis binds have been identified, including salivary immunoglobulin A and ␣-amylase (27).…”

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confidence: 99%

“…Studies employing saliva-coated hydroxyapatite as a tooth model have revealed both lectin-carbohydrate and nonlectin interactions (27,38,42,64). Some of the salivary components to which S. sanguinis binds have been identified, including salivary immunoglobulin A and ␣-amylase (27). Once bound, S. sanguinis serves as a tether for the attachment of other oral microorganisms that colonize the tooth surface, form dental plaque, and contribute to development of caries and periodontal disease (46).…”

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confidence: 99%

Genome of the Opportunistic Pathogen Streptococcus sanguinis

et al. 2007

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The genome of Streptococcus sanguinis is a circular DNA molecule consisting of 2,388,435 bp and is 177 to 590 kb larger than the other 21 streptococcal genomes that have been sequenced. The G؉C content of the S. sanguinis genome is 43.4%, which is considerably higher than the G؉C contents of other streptococci. The genome encodes 2,274 predicted proteins, 61 tRNAs, and four rRNA operons. A 70-kb region encoding pathways for vitamin B 12 biosynthesis and degradation of ethanolamine and propanediol was apparently acquired by horizontal gene transfer. The gene complement suggests new hypotheses for the pathogenesis and virulence of S. sanguinis and differs from the gene complements of other pathogenic and nonpathogenic streptococci. In particular, S. sanguinis possesses a remarkable abundance of putative surface proteins, which may permit it to be a primary colonizer of the oral cavity and agent of streptococcal endocarditis and infection in neutropenic patients.

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Salivary Film Expresses a Complex, Macromolecular Binding Site for Streptococcus sanguis

Cited by 44 publications

References 29 publications

Adhesion of Streptococcus sanguinis to Dental Implant and Restorative Materials in vitro

Adhesion of Streptococcus sanguinis to Dental Implant and Restorative Materials in vitro

Involvement of Streptococcus gordonii Beta-Glucoside Metabolism Systems in Adhesion, Biofilm Formation, and In Vivo Gene Expression

Genome of the Opportunistic Pathogen Streptococcus sanguinis

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