Cariogenic potential in vitro in man and in vivo in the rat of lactate dehydrogenase mutants of Streptococcus mutans

Johnson, Christine P.; Gross, Steffen; Hillman, Jeffrey D.

doi:10.1016/0003-9969(80)90124-7

Cited by 47 publications

(41 citation statements)

References 17 publications

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“…mutans contains glycolytic pathway which produce lactate, formate, acetate, and ethanol as fermentation products [91]. Strains deficient in lactate dehydrogenase (LDH) display reduced cariogenicity [92,93] and the dearth of lactate dehydrogenase (LDH) is lethal. The acidogenicity of S. mutans leads to ecological changes in the plaque flora that includes an elevation in the proportion of S. mutans and other acidogenic and acid-tolerant species ( Figure 4).…”

Section: Acidogenicitymentioning

confidence: 99%

Dental Caries: A Microbiological Approach

Yadav¹,

Prakash²

2017

J Clin Infect Dis Pract

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Section: Acidogenicitymentioning

confidence: 99%

Dental Caries: A Microbiological Approach

Yadav¹,

Prakash²

2017

J Clin Infect Dis Pract

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“…Cariogenic virulence factors of S. mutans lead to abundant acid production, acid tolerance and stable biofilm formation [2]. Production of acid during metabolism of carbohydrates (acidogenicity) is one of the main virulence factors of S. mutans , in which lactate dehydrogenase (LDH) plays a critical role [3]. Aciduricity is also a pivotal virulence factor of S. mutans .…”

Section: Introductionmentioning

confidence: 99%

Antimicrobial peptide GH12 suppresses cariogenic virulence factors of Streptococcus mutans

Wang

Jiang

et al. 2018

Journal of Oral Microbiology

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Cariogenic virulence factors of Streptococcus mutans include acidogenicity, aciduricity, and extracellular polysaccharides (EPS) synthesis. The de novo designed antimicrobial peptide GH12 has shown bactericidal effects on S. mutans, but its interaction with virulence and regulatory systems of S. mutans remains to be elucidated. The objectives were to investigate the effects of GH12 on virulence factors of S. mutans, and further explore the function mechanisms at enzymatic and transcriptional levels. To avoid decrease in bacterial viability, we limited GH12 to subinhibitory levels. We evaluated effects of GH12 on acidogenicity of S. mutans by pH drop, lactic acid measurement and lactate dehydrogenase (LDH) assay, on aciduricity through survival rate at pH 5.0 and F1F0-ATPase assay, and on EPS synthesis using quantitative measurement, morphology observation, vertical distribution analyses and biomass calculation. Afterwards, we conducted quantitative real-time PCR to acquire the expression profile of related genes. GH12 at 1/2 MIC (4 mg/L) inhibited acid production, survival rate, EPS synthesis, and biofilm formation. The enzymatic activity of LDH and F1F0-ATPase was inhibited, and ldh, gtfBCD, vicR, liaR, and comDE genes were significantly downregulated. In conclusion, GH12 inhibited virulence factors of S. mutans, through reducing the activity of related enzymes, downregulating virulence genes, and inactivating specific regulatory systems.

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“…Since acid production by mutans streptococci has long been known to be integral to the pathogenic process, effector strains with low acid-producing capabilities have been sought (1,8,29). Lactate dehydrogenase (LDH)-deficient mutants of Streptococcus rattus were shown to have little or no cariogenic potential in vitro and in various rodent models (18).…”

mentioning

confidence: 99%

Construction and Characterization of an Effector Strain of Streptococcus mutans for Replacement Therapy of Dental Caries

et al. 2000

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An effector strain has been constructed for use in the replacement therapy of dental caries. Recombinant DNA methods were used to make the Streptococcus mutans supercolonizing strain, JH1140, lactate dehydrogenase deficient by deleting virtually all of the ldh open reading frame (ORF). To compensate for the resulting metabolic imbalance, a supplemental alcohol dehydrogenase activity was introduced by substituting the adhB ORF from Zymomonas mobilis in place of the deleted ldh ORF. The resulting clone, BCS3-L1, was found to produce no detectable lactic acid during growth on a variety of carbon sources, and it produced significantly less total acid due to its increased production of ethanol and acetoin. BCS3-L1 was significantly less cariogenic than JH1140 in both gnotobiotic-and conventional-rodent models. It colonized the teeth of conventional rats as well as JH1140 in both aggressive-displacement and preemptive-colonization models. No gross or microscopic abnormalities of major organs were associated with oral colonization of rats with BCS3-L1 for 6 months. Acid-producing revertants of BCS3-L1 were not observed in samples taken from infected animals (reversion frequency, <10 ؊3 ) or by screening cultures grown in vitro, where no revertants were observed among 10 5 colonies examined on pH indicator medium. The reduced pathogenic potential of BCS3-L1, its strong colonization potential, and its genetic stability suggest that this strain is well suited to serve as an effector strain in the replacement therapy of dental caries in humans.

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Cariogenic potential in vitro in man and in vivo in the rat of lactate dehydrogenase mutants of Streptococcus mutans

Cited by 47 publications

References 17 publications

Dental Caries: A Microbiological Approach

Dental Caries: A Microbiological Approach

Antimicrobial peptide GH12 suppresses cariogenic virulence factors of Streptococcus mutans

Construction and Characterization of an Effector Strain of Streptococcus mutans for Replacement Therapy of Dental Caries

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