Acid‐adaptive mechanisms of <i>Streptococcus mutans</i>–the more we know, the more we don't

Baker, Jonathon L.; Faustoferri, Roberta C.; Quivey, Robert G.

doi:10.1111/omi.12162

Cited by 96 publications

(86 citation statements)

References 83 publications

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“…In addition to an increase in the UFA:SFA ratio, another major component of the S. mutans ATR is increased expression and activity of the F 1 F 0 ‐ATPase (Baker et al, ; Kuhnert et al, ). This complex hydrolyzes ATP to extrude protons from the cell interior in order to maintain a relatively alkaline cytoplasm during growth of the organism in acidic conditions (Kuhnert et al, ).…”

Section: Resultsmentioning

confidence: 99%

“…Microarray analysis also indicated that SpxA2 may be a repressor of the operon encoding the F 1 F 0 ATPase (Kajfasz et al, ), which is another crucial component of the S. mutans ATR (Baker et al, ). We confirmed that ATPase activity was indeed significantly increased in the ∆ spxA2 strain concurrent with the increased transcriptional expression (Figure ).…”

Section: Discussionmentioning

confidence: 99%

“…S. mutans contributes substantially to caries pathogenesis through its exceptional capacity to form biofilms and its ability to produce acid from a wide variety of carbohydrate sources (Bowen, Burne, Wu, & Koo, ; Lemos et al, ). Furthermore, S. mutans employs an acid‐tolerance response (ATR) that utilizes multiple mechanisms to survive better in acidic conditions than many of its neighbors in the oral microbiota (Baker, Faustoferri, & Quivey, ; Lemos & Burne, ). This allows S. mutans to contribute to the destruction of the underlying tooth even at low pH values that would arrest growth and glycolysis in many more benign species.…”

Section: Introductionmentioning

confidence: 99%

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Streptococcus mutans SpxA2 relays the signal of cell envelope stress from LiaR to effectors that maintain cell wall and membrane homeostasis

Baker

Saputo

Faustoferri

et al. 2020

Molecular Oral Microbiology

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Streptococcus mutans is a major etiologic agent of dental caries, which is the most common chronic infectious disease worldwide. S. mutans is particularly adept at causing caries due to its exceptional capacity to form biofilms and its ability to survive acidic conditions that arrest acid production and growth in many more benign members of the oral microbiota. Two mechanisms utilized by S. mutans to tolerate acid are: modulation of the membrane fatty acid content and utilization of the F 1 F 0 -ATPase to pump protons out of the cytosol. In this study, the role of the spxA2 transcriptional regulator in these two pathways, and overall cell envelope homeostasis, was examined. Loss of spxA2 resulted in an increase in the proportion of saturated fatty acids in the S. mutans membrane and altered transcription of several genes involved in the production of these membrane fatty acids, including fabT and fabM. Furthermore, activity of the F 1 F 0 -ATPase was increased in the ∆spxA2 strain. Transcription of spxA2 was elevated in the presence of a variety of membrane stressors, and highly dependent on the liaR component of the LiaFSR system, which is known to sense cell envelope stress in many Gram-positive bacteria. Finally, deletion of ∆spxA2 led to altered susceptibility of S. mutans to membrane stressors. Overall, the results of this study indicate that spxA2 serves a crucial role in transmitting the signal of cell wall/membrane damage from the LiaFSR sensor to downstream effectors in the SpxA2 regulon which restore and maintain membrane and cell wall homeostasis.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Streptococcus mutans SpxA2 relays the signal of cell envelope stress from LiaR to effectors that maintain cell wall and membrane homeostasis

Baker

Saputo

Faustoferri

et al. 2020

Molecular Oral Microbiology

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“…how many taxa contribute a particular pathway to the community)(34) was reduced in the caries group. This was particularly evident in the aerobic respiration performed by the health-associated Neisseria, and several pathways that have been previously associated with the forestalling of caries pathogenesis including arginine (35) and BCAA pathways (37), which both release alkaline molecules that serve to buffer the environment and prevent enamel demineralization (63).…”

Section: Discussionmentioning

confidence: 99%

Deep metagenomics examines the oral microbiome during dental caries, revealing novel taxa and co-occurrences with host molecules

Baker

Morton

Dinis³

et al. 2019

Preprint

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45Dental caries is the most common chronic infectious disease globally. The microbial communities 46 associated with caries have mainly been examined using relatively low-resolution 16S rRNA gene 47 amplicon sequencing and/or using downstream analyses that are unsound for the compositional 48 nature of the data provided by sequencing. Additionally, the relationship between caries, oral 49 microbiome composition, and host immunological markers has not been explored. In this study, 50 the oral microbiome and a panel of 38 host markers was analyzed across the saliva from 23 51 children with dentin caries and 24 children with healthy dentition. Metagenomic sequencing, 52 followed by investigation using tools designed to be robust for compositional data, illustrated 53 that several Prevotella spp. were prevalent in caries, while Rothia spp. were associated with the 54 health. The contributional diversity (extent to which multiple taxa contribute to each pathway) 55 of functional pathways present in the oral microbiome was decreased in the caries group. This 56 decrease was especially noticeable in several pathways known to impede caries pathogenesis, 57 including arginine and branched-chain amino acid biosynthesis. 10 host immunological markers 58 were found to be significantly elevated in the saliva of the caries group, and microbe-metabolite 59 co-occurrence analysis provided an atlas of relationships contributing to the bi-directional 60 influence between the oral microbiome and the host immune system. Finally, 527 metagenome-61 assembled genomes were obtained from the metagenomics data, representing 151 species. 23 62 taxa were novel genera/species and a further 20 taxa were novel species. This study thus serves 63 as a model analysis pipeline that will tremendously expand our knowledge of the oral microbiome 64 and its relationship to dental caries once applied to large populations. 65 67Dental caries is the most common chronic infectious disease and will afflict well over half of the 68 global human population at some point in their lives. Dental caries is particularly problematic in 69 children, where it is five times more common than asthma, the second most common chronic 70 disease. This extreme prevalence translates to an extraordinary economic burden. Caries 71 disproportionally afflicts vulnerable populations least able to access and afford proper treatment 72(1). Historically, members of the acid-producing and acid-tolerant mutans group of streptococci, 73 particularly the paradigm species of the group, Streptococcus mutans, were considered the 74 etiologic agents of the disease (2). While caries is certainly an infectious and transmissible 75 disease caused by the oral microbiota, it is now understood to be multifactorial and ecology-76 based, because although mutans streptococci are commonly associated with caries, they are 77 neither necessary nor sufficient to cause disease (3). Interplay between host genetic and 78 immunological factors, diet and hygiene habits, and the oral microbiota affect clinica...

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“…Streptococcus mutans is considered a major etiologic agent contributing to the initiation and the progression of dental caries (6). One primary virulence attribute of S. mutans is extreme acidification of the environment from the fermentation of an array of carbohydrates (7,8). Another determining factor that enables S. mutans to become a successful cariogenic bacterium is its exceptional capacity to form biofilms on teeth, largely facilitated by its robust production of extracellular polymeric substances (EPS) catalyzed by secreted glucosyltransferases (Gtfs) and fructosyltransferase (Ftf) enzymes that generate diffusion-limiting exopolysaccharides (6), and the ability to produce substantial quantities of extracellular DNA (eDNA) (9).…”

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confidence: 99%

Amino Sugars Modify Antagonistic Interactions between Commensal Oral Streptococci and Streptococcus mutans

Chen

Chakraborty

Zou

et al. 2019

Appl Environ Microbiol

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N-Acetylglucosamine (GlcNAc) and glucosamine (GlcN) enhance the competitiveness of the laboratory strain DL1 of Streptococcus gordonii against the caries pathogen Streptococcus mutans. Here, we examine how amino sugars affect the interaction of five low-passage-number clinical isolates of abundant commensal streptococci with S. mutans by utilizing a dual-species biofilm model. Compared to that for glucose, growth on GlcN or GlcNAc significantly reduced the viability of S. mutans in cocultures with most commensals, shifting the proportions of species. Consistent with these results, production of H 2 O 2 was increased in most commensals when growing on amino sugars, and inhibition of S. mutans by Streptococcus cristatus, Streptococcus oralis, or S. gordonii was enhanced by amino sugars on agar plates. All commensals except S. oralis had higher arginine deiminase activities when grown on GlcN and, in some cases, GlcNAc. In ex vivo biofilms formed using pooled cell-containing saliva (CCS), the proportions of S. mutans were drastically diminished when GlcNAc was the primary carbohydrate. Increased production of H 2 O 2 could account in large part for the inhibitory effects of CCS biofilms. Surprisingly, amino sugars appeared to improve mutacin production by S. mutans on agar plates, suggesting that the commensals have mechanisms to actively subvert antagonism by S. mutans in cocultures. Collectively, these findings demonstrate that amino sugars can enhance the beneficial properties of low-passage-number commensal oral streptococci and highlight their potential for moderating the cariogenicity of oral biofilms. IMPORTANCE Dental caries is driven by dysbiosis of oral biofilms in which dominance by acid-producing and acid-tolerant bacteria results in loss of tooth mineral. Our previous work demonstrated the beneficial effects of amino sugars GlcNAc and GlcN in promoting the antagonistic properties of a health-associated oral bacterium, Streptococcus gordonii, in competition with the major caries pathogen Streptococcus mutans. Here, we investigated 5 low-passage-number clinical isolates of the most common streptococcal species to establish how amino sugars may influence the ecology and virulence of oral biofilms. Using multiple in vitro models, including a human saliva-derived microcosm biofilm, experiments showed significant enhancement by at least one amino sugar in the ability of most of these bacteria to suppress the caries pathogen. Therefore, our findings demonstrated the mechanism of action by which amino sugars may affect human oral biofilms to promote health.

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Acid‐adaptive mechanisms of Streptococcus mutans–the more we know, the more we don't

Cited by 96 publications

References 83 publications

Streptococcus mutans SpxA2 relays the signal of cell envelope stress from LiaR to effectors that maintain cell wall and membrane homeostasis

Streptococcus mutans SpxA2 relays the signal of cell envelope stress from LiaR to effectors that maintain cell wall and membrane homeostasis

Deep metagenomics examines the oral microbiome during dental caries, revealing novel taxa and co-occurrences with host molecules

Amino Sugars Modify Antagonistic Interactions between Commensal Oral Streptococci and Streptococcus mutans

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