scholarly journals Prevention of Streptococcus mutans infection of tooth surfaces by salivary antibody in Irus monkeys (Macaca fascicularis).

1975 ◽  
Vol 12 (2) ◽  
pp. 293-302 ◽  
Author(s):  
R T Evans ◽  
F G Emmings ◽  
R J Genco
Keyword(s):  
Streptococcus Mutans ◽  
Macaca Fascicularis ◽  
Tooth Surfaces

scholarly journals Exopolysaccharides Produced by Streptococcus mutans Glucosyltransferases Modulate the Establishment of Microcolonies within Multispecies Biofilms

2010 ◽  
Vol 192 (12) ◽  
pp. 3024-3032 ◽  
Author(s):  
H. Koo ◽  
J. Xiao ◽  
M. I. Klein ◽  
J. G. Jeon
Keyword(s):  
Streptococcus Mutans ◽  
Extracellular Polysaccharide ◽  
Fluorescence Labeling ◽  
Tooth Surface ◽  
Bacterial Cells ◽  
Actinomyces Naeslundii ◽  
Multispecies Biofilm ◽  
Tooth Surfaces ◽  
Glucan Synthesis

ABSTRACT Streptococcus mutans is a key contributor to the formation of the extracellular polysaccharide (EPS) matrix in dental biofilms. The exopolysaccharides, which are mostly glucans synthesized by streptococcal glucosyltransferases (Gtfs), provide binding sites that promote accumulation of microorganisms on the tooth surface and further establishment of pathogenic biofilms. This study explored (i) the role of S. mutans Gtfs in the development of the EPS matrix and microcolonies in biofilms, (ii) the influence of exopolysaccharides on formation of microcolonies, and (iii) establishment of S. mutans in a multispecies biofilm in vitro using a novel fluorescence labeling technique. Our data show that the ability of S. mutans strains defective in the gtfB gene or the gtfB and gtfC genes to form microcolonies on saliva-coated hydroxyapatite surfaces was markedly disrupted. However, deletion of both gtfB (associated with insoluble glucan synthesis) and gtfC (associated with insoluble and soluble glucan synthesis) is required for the maximum reduction in EPS matrix and biofilm formation. S. mutans grown with sucrose in the presence of Streptococcus oralis and Actinomyces naeslundii steadily formed exopolysaccharides, which allowed the initial clustering of bacterial cells and further development into highly structured microcolonies. Concomitantly, S. mutans became the major species in the mature biofilm. Neither the EPS matrix nor microcolonies were formed in the presence of glucose in the multispecies biofilm. Our data show that GtfB and GtfC are essential for establishment of the EPS matrix, but GtfB appears to be responsible for formation of microcolonies by S. mutans; these Gtf-mediated processes may enhance the competitiveness of S. mutans in the multispecies environment in biofilms on tooth surfaces.

scholarly journals Proteome Analysis Identifies the Dpr Protein of Streptococcus mutans as an Important Factor in the Presence of Early Streptococcal Colonizers of Tooth Surfaces

PLoS ONE ◽  
2015 ◽  
Vol 10 (3) ◽  
pp. e0121176 ◽  
Author(s):  
Akihiro Yoshida ◽  
Mamiko Niki ◽  
Yuji Yamamoto ◽  
Ai Yasunaga ◽  
Toshihiro Ansai
Keyword(s):  
Streptococcus Mutans ◽  
Proteome Analysis ◽  
Tooth Surfaces

scholarly journals Pleiotropic Regulation of Virulence Genes in Streptococcus mutans by the Conserved Small Protein SprV

2017 ◽  
Vol 199 (8) ◽  
Author(s):  
Manoharan Shankar ◽  
Mohammad S. Hossain ◽  
Indranil Biswas
Keyword(s):  
Dental Caries ◽  
Streptococcus Mutans ◽  
Virulence Factors ◽  
Biofilm Formation ◽  
Normal Growth ◽  
Hypothetical Protein ◽  
Bacteriocin Production ◽  
Transcript Levels ◽  
Content Type ◽  
Tooth Surfaces

ABSTRACT Streptococcus mutans, an oral pathogen associated with dental caries, colonizes tooth surfaces as polymicrobial biofilms known as dental plaque. S. mutans expresses several virulence factors that allow the organism to tolerate environmental fluctuations and compete with other microorganisms. We recently identified a small hypothetical protein (90 amino acids) essential for the normal growth of the bacterium. Inactivation of the gene, SMU.2137, encoding this protein caused a significant growth defect and loss of various virulence-associated functions. An S. mutans strain lacking this gene was more sensitive to acid, temperature, osmotic, oxidative, and DNA damage-inducing stresses. In addition, we observed an altered protein profile and defects in biofilm formation, bacteriocin production, and natural competence development, possibly due to the fitness defect associated with SMU.2137 deletion. Transcriptome sequencing revealed that nearly 20% of the S. mutans genes were differentially expressed upon SMU.2137 deletion, thereby suggesting a pleiotropic effect. Therefore, we have renamed this hitherto uncharacterized gene as sprV (streptococcal pleiotropic regulator of virulence). The transcript levels of several relevant genes in the sprV mutant corroborated the phenotypes observed upon sprV deletion. Owing to its highly conserved nature, inactivation of the sprV ortholog in Streptococcus gordonii also resulted in poor growth and defective UV tolerance and competence development as in the case of S. mutans. Our experiments suggest that SprV is functionally distinct from its homologs identified by structure and sequence homology. Nonetheless, our current work is aimed at understanding the importance of SprV in the S. mutans biology. IMPORTANCE Streptococcus mutans employs several virulence factors and stress resistance mechanisms to colonize tooth surfaces and cause dental caries. Bacterial pathogenesis is generally controlled by regulators of fitness that are critical for successful disease establishment. Sometimes these regulators, which are potential targets for antimicrobials, are lost in the genomic context due to the lack of annotated homologs. This work outlines the regulatory impact of a small, highly conserved hypothetical protein, SprV, encoded by S. mutans. We show that SprV affects the transcript levels of various virulence factors required for normal growth, biofilm formation, stress tolerance, genetic competence, and bacteriocin production.

scholarly journals Characterization of Salivary Immunoglobulin A Responses in Children Heavily Exposed to the Oral Bacterium Streptococcus mutans: Influence of Specific Antigen Recognition in Infection

2005 ◽  
Vol 73 (9) ◽  
pp. 5675-5684 ◽  
Author(s):  
Ruchele D. Nogueira ◽  
Alessandra C. Alves ◽  
Marcelo H. Napimoga ◽  
Daniel J. Smith ◽  
Renata O. Mattos-Graner
Keyword(s):  
Streptococcus Mutans ◽  
Specific Antigen ◽  
Immunoglobulin A ◽  
Salivary Iga ◽  
Racial Background ◽  
Tooth Surfaces ◽  
Natural Response ◽  
Iga Antibody ◽  
Antibody Specificities ◽  
Salivary Immunoglobulin A

ABSTRACT The initial infection of children by Streptococcus mutans, the main pathogen of dental caries, depends on the ability of S. mutans to adhere and accumulate on tooth surfaces. These processes involve the adhesin antigen I/II (AgI/II), glucosyltransferases (GTF) and glucan-binding protein B (GbpB), each a target for anticaries vaccines. The salivary immunoglobulin A (IgA) antibody responses to S. mutans antigens (Ags) were characterized in 21 pairs of 5- to 13-month-old children. Pairs were constructed with one early S. mutans-infected and one noninfected child matched by age, racial background, number of teeth, and salivary levels of IgA. Specific salivary IgA antibody response and S. mutans infection levels were then measured during a 1-year follow-up. Robust responses to S. mutans were detected from 6 months of age. Salivary IgA antibody to AgI/II and GTF was commonly detected in salivas of all 42 children. However, GbpB-specific IgA antibody was seldom detected in the subset of infected children (38.1% at baseline). In contrast, most of the subset of noninfected children (76.2%) showed GbpB-reactive IgA antibody during the same period. Frequencies of GbpB responses increased with age, but differences in intensities of GbpB-IgA antibody reactions were sustained between the subsets. At baseline, GbpB-reactive IgA antibody accounted for at least half of the total salivary IgA S. mutans-reactive antibody in 33.3 and 9.5% of noninfected and infected children, respectively. This study provides evidence that a robust natural response to S. mutans Ags can be achieved by 1 year of age and that IgA antibody specificities may be critical in modulating initial S. mutans infection.

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