&lt;b&gt;&lt;i&gt;Streptococcus mutans&lt;/i&gt;&lt;/b&gt; and &lt;b&gt;&lt;i&gt;Streptococcus sanguinis&lt;/i&gt;&lt;/b&gt; Expression of Competition-Related Genes, Under Sucrose

Lozano, Carla; Díaz-Garrido, Natalia; Kreth, Jens; Giacaman, Rodrigo A.

doi:10.1159/000490950

Cited by 16 publications

(11 citation statements)

References 46 publications

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“…The expression of virulence genes associated with these species and their molecular mechanisms have been studied. Previously, our research group analyzed the transcriptional expression of the gtf genes of both bacteria and the spxB gene of S. sanguinis using the same experimental approach and design than that of this article (22). Interestingly, all genes were overexpressed when either species acted as the invading microorganism over an already formed biofilm by the antagonistic species, arguably in an attempt to colonize.…”

Section: Discussionmentioning

confidence: 99%

Competition and Caries on Enamel of a Dual-Species Biofilm Model with Streptococcus mutans and Streptococcus sanguinis

Díaz-Garrido

Lozano

Kreth

et al. 2020

Appl Environ Microbiol

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Imbalances within the dental biofilm trigger dental caries, currently considered a dysbiosis and the most prevalent non-communicable disease. There is still a gap in knowledge about the dynamics of enamel colonization by bacteria from the dental biofilm in caries. The aim, therefore, was to test whether the sequence of enamel colonization by a typically commensal and a cariogenic species modifies biofilm's cariogenicity. Dual-species biofilms of Streptococcus mutans (Sm) and Streptococcus sanguinis (Ss) on saliva-coated enamel slabs were inoculated in different sequences: Sm followed by Ss (Sm-Ss), Ss followed by Sm (Ss-Sm), Sm and Ss inoculated at the same time (Sm=Ss) and the single-species controls Sm followed by Sm (Sm-Sm) and Ss followed by Ss (Ss-Ss). Biofilms were exposed to 10% sucrose, 3x/day for 5 days and the slabs/biofilms were retrieved to assess demineralization, viable cells, biomass, proteins, polysaccharides and H2O2 production. When compared with Sm-Sm, primary inoculation with Ss reduced demineralization (p<0.05). Both Ss-Sm and Sm=Ss sequences showed reduction in biomass, protein and polysaccharide content (p<0.05). The highest S. sanguinis viable cells and H2O2 production and the lowest acidogenicity were observed when Ss colonized enamel before Sm (p<0.05). Initial enamel adherence with commensal biofilms seems to induce more intense competition against more typically cariogenic species, reducing cariogenicity. Importance The concept of caries as an ecological disease implies the understanding of the intricate relationships among the populating microorganisms. Under frequent sugars exposure, some bacteria from the dental biofilm develop pathogenic traits that lead to imbalances (dysbiosis). Depending on which microorganism colonizes the dental surface first, different competition strategies may be developed. Studying the interactions in the entire dental biofilm is not an easy task. In this article, therefore, we modeled the interplay among these microorganisms using a caries-inducing (S. mutans) and a health-associated species (S. sanguinis). Initial enamel adherence with S. sanguinis seems to induce more intense competition against typically caries-inducing species. Besides continuous exposure with sugars, early colonization of the enamel by highly cariogenic species, like S. mutans, appears to be needed to develop caries lesions, as well. Promoting early colonization by health-associated bacteria, such as S. sanguinis, could help to maintain oral health, delaying dysbiosis.

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Section: Discussionmentioning

confidence: 99%

Competition and Caries on Enamel of a Dual-Species Biofilm Model with Streptococcus mutans and Streptococcus sanguinis

Díaz-Garrido

Lozano

Kreth

et al. 2020

Appl Environ Microbiol

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“…Thus, there was a downregulation of the GTFs genes during simultaneous biofilm formation, but an upregulation of gtfB, gtfC and gtf D when S. sanguinis was the first colonizer and an upregulation of S. sanguinis gtfP (encoding GtfS) when S. mutans was the initial colonizer. 34 Based on the biomass data and under the conditions tested here, S. sanguinis could become only moderately cariogenic if allowed to colonize for longer periods and frequently exposed to sucrose. Caries has been reported in the absence of cariogenic S. mutans and our findings might explain why other species are able to produce acid through fermentation, which could be responsible for this observation.…”

Section: Discussionmentioning

confidence: 78%

Extended biofilm formation time by Streptococcus sanguinis modifies its non-cariogenic behavior, in vitro

et al. 2022

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Although the commensal Streptococcus sanguinis [S. sanguinis] is isolated from caries-free people, it can ferment carbohydrates producing acids. We aimed to characterize S. sanguinis cariogenic potential as a function of different enamel biofilm formation periods, in vitro. Saliva-coated enamel slabs were inoculated with S. sanguinis to form initial biofilms for 8, 12 or 16 h in presence of sucrose and followed by a period in medium with glucose for 16, 12 or 8 h, respectively, until completion of 24 h. To simulate cariogenic challenges, S. sanguinis biofilms were exposed to 10% sucrose for 5 minutes, 3x/day for 5 days. Biofilm biomass, viable cells, total proteins, intracellular and extracellular polysaccharides production, acidogenicity and enamel demineralization were determined. Biofilms of Streptococcus mutans [S. mutans] served as caries-positive control. Biofilms of S. sanguinis forming on enamel for 12 and 16 h showed higher demineralization than those formed during 8 h, but lower than S. mutans biofilms, regardless of the initial biofilm formation time. No differences were detected in the biofilm properties among the different biofilm formation times tested for S. sanguinis. Increased enamel initial biofilm formation time by S. sanguinis appears to induce a cariogenic potential, but lower than S. mutans.

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“…Both S. gordonii and S. sanguinis are capable of producing hydrogen peroxide that inhibits the growth of S. mutans (Huang et al., 2018; Kreth et al., 2008; Lozano et al., 2019; Mu et al., 2021); thus, we performed a hydrogen peroxide tolerance experiment to verify the tolerance of S. mutans and its derivatives to hydrogen peroxide. There was no significant difference in the zone of inhibition of S. mutans and its derivatives (Figure S3A,B).…”

Section: Resultsmentioning

confidence: 99%

vicR overexpression in Streptococcus mutans causes aggregation and affects interspecies competition

Yan

Gong

et al. 2023

Molecular Oral Microbiology

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Streptococcus mutans is considered to be a major causative agent of dental caries. VicRK is a two‐component signal transduction system (TCSTS) of S. mutans, which can regulate the virulence of S. mutans, such as biofilm formation, exopolysaccharide production, acid production, and acid resistance. Meanwhile, it can also regulate the production of mutacins (nlmC) through the TCSTS ComDE. In this study, we found that the vicR‐overexpressing strain was more likely to aggregate to form cell clusters, leading to the formation of abnormal biofilm; the overexpression of vicR increased the length of the chain of S. mutans. Furthermore, the expression of the mutacins in the vicR overexpression strain was increased under aerobic conditions. Compared with the control strain and the parental strain, the vicR overexpression strain was more competitive against Streptococcus gordonii. But there was no significant difference against Streptococcus sanguinis. In clinical strains, the expression level of vicR was positively correlated with their competitive ability against S. gordonii. Transcriptional profiling revealed 24 significantly upregulated genes in the vicR‐overexpressing strain, including nlmA, nlmB, nlmC, and nlmD encoding mutacins. Electrophoretic mobility shift assays and DNase I footprinting assays confirmed that VicR can directly bind to the promoter sequence of nlmD. Taken together, our findings further demonstrate that VicRK, an important TCSTS of S. mutans, is involved in S. mutans cell morphology and biofilm formation. VicRK regulates the production of more mutacins in S. mutans in response to oxygen stimulation. VicR can bind to the promoter sequence of nlmD, thereby directly regulating the production of mutacins NlmD.

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<b><i>Streptococcus mutans</i></b> and <b><i>Streptococcus sanguinis</i></b> Expression of Competition-Related Genes, Under Sucrose

Cited by 16 publications

References 46 publications

Competition and Caries on Enamel of a Dual-Species Biofilm Model with Streptococcus mutans and Streptococcus sanguinis

Competition and Caries on Enamel of a Dual-Species Biofilm Model with Streptococcus mutans and Streptococcus sanguinis

Extended biofilm formation time by Streptococcus sanguinis modifies its non-cariogenic behavior, in vitro

vicR overexpression in Streptococcus mutans causes aggregation and affects interspecies competition

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