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1
Brown, Alan E., Jeffrey D. Rogers, Elaine M. Haase, Peter M. Zelasko, and Frank A. Scannapieco. "Prevalence of the Amylase-Binding Protein A Gene (abpA) in Oral Streptococci." Journal of Clinical Microbiology 37, no. 12 (1999): 4081–85. http://dx.doi.org/10.1128/jcm.37.12.4081-4085.1999.
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Salivary amylase binds specifically to a number of oral streptococcal species. This interaction may play an important role in dental plaque formation. Recently, a 585-bp gene was cloned and sequenced from Streptococcus gordonii Challis encoding a 20.5-kDa amylase-binding protein (AbpA). The goal of this study was to determine if related genes are present in other species of oral streptococci. Biotinylated abpA was used in Southern blot analysis to screen genomic DNA from several strains representing eight species of oral streptococci. This probe hybridized with a 4.0-kbHindIII restriction fragment from all 13 strains ofS. gordonii tested. The probe did not appear to bind to any restriction fragments from other species of amylase-binding oral streptococci including Streptococcus mitis (with the exception of 1 of 14 strains), Streptococcus crista (3 strains), Streptococcus anginosus (1 strain), andStreptococcus parasanguinis (1 strain), or to non-amylase-binding oral streptococci including Streptococcus sanguinis (3 strains), Streptococcus oralis (4 strains), and Streptococcus mutans (1 strain). Primers homologous to sequences within the 3′ and 5′ ends of abpAyielded products of 400 bp following PCR of genomic DNA from the Southern blot-positive strains. Several of these PCR products were cloned and sequenced. The levels of similarity of these cloned products to the abpA of S. gordonii Challis ranged from 91 to 96%. These studies reveal that the abpA gene appears to be specific to S. gordonii and differs from genes encoding amylase-binding proteins from other species of amylase-binding streptococci.
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Kreth, Jens, Yongshu Zhang, and Mark C. Herzberg. "Streptococcal Antagonism in Oral Biofilms: Streptococcus sanguinis and Streptococcus gordonii Interference with Streptococcus mutans." Journal of Bacteriology 190, no. 13 (April 25, 2008): 4632–40. http://dx.doi.org/10.1128/jb.00276-08.
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ABSTRACT Biofilms are polymicrobial, with diverse bacterial species competing for limited space and nutrients. Under healthy conditions, the different species in biofilms maintain an ecological balance. This balance can be disturbed by environmental factors and interspecies interactions. These perturbations can enable dominant growth of certain species, leading to disease. To model clinically relevant interspecies antagonism, we studied three well-characterized and closely related oral species, Streptococcus gordonii, Streptococcus sanguinis, and cariogenic Streptococcus mutans. S. sanguinis and S. gordonii used oxygen availability and the differential production of hydrogen peroxide (H2O2) to compete effectively against S. mutans. Interspecies antagonism was influenced by glucose with reduced production of H2O2. Furthermore, aerobic conditions stimulated the competence system and the expression of the bacteriocin mutacin IV of S. mutans, as well as the H2O2-dependent release of heterologous DNA from mixed cultures of S. sanguinis and S. gordonii. These data provide new insights into ecological factors that determine the outcome of competition between pioneer colonizing oral streptococci and the survival mechanisms of S. mutans in the oral biofilm.
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Cheng, X., S. Redanz, P. Treerat, H. Qin, D. Choi, X. Zhou, X. Xu, J. Merritt, and J. Kreth. "Magnesium-Dependent Promotion of H2O2 Production Increases Ecological Competitiveness of Oral Commensal Streptococci." Journal of Dental Research 99, no. 7 (March 20, 2020): 847–54. http://dx.doi.org/10.1177/0022034520912181.
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The pyruvate oxidase (SpxB)–dependent production of H2O2 is widely distributed among oral commensal streptococci. Several studies confirmed the ability of H2O2 to antagonize susceptible oral bacterial species, including caries-associated Streptococcus mutans as well as several periodontal pathobionts. Here we report a potential mechanism to bolster oral commensal streptococcal H2O2 production by magnesium (Mg2+) supplementation. Magnesium is a cofactor for SpxB catalytic activity, and supplementation increases the production of H2O2 in vitro. We demonstrate that Mg2+ affects spxB transcription and SpxB abundance in Streptococcus sanguinis and Streptococcus gordonii. The competitiveness of low-passage commensal streptococcal clinical isolates is positively influenced in antagonism assays against S. mutans. In growth conditions normally selective for S. mutans, Mg2+ supplementation is able to increase the abundance of S. sanguinis in dual-species biofilms. Using an in vivo biophotonic imaging platform, we further demonstrate that dietary Mg2+ supplementation significantly improves S. gordonii oral colonization in mice. In summary, our results support a role for Mg2+ supplementation as a potential prebiotic to promote establishment of oral health–associated commensal streptococci.
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Ashby, Michael T., Jens Kreth, Muthu Soundarajan, and Laure Sita Sivuilu. "Influence of a model human defensive peroxidase system on oral streptococcal antagonism." Microbiology 155, no. 11 (November 1, 2009): 3691–700. http://dx.doi.org/10.1099/mic.0.031310-0.
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Streptococcus is a dominant genus in the human oral cavity, making up about 20 % of the more than 800 species of bacteria that have been identified, and about 80 % of the early biofilm colonizers. Oral streptococci include both health-compatible (e.g. Streptococcus gordonii and Streptococcus sanguinis) and pathogenic strains (e.g. the cariogenic Streptococcus mutans). Because the streptococci have similar metabolic requirements, they have developed defence strategies that lead to antagonism (also known as bacterial interference). S. mutans expresses bacteriocins that are cytotoxic toward S. gordonii and S. sanguinis, whereas S. gordonii and S. sanguinis differentially produce H2O2 (under aerobic growth conditions), which is relatively toxic toward S. mutans. Superimposed on the inter-bacterial combat are the effects of the host defensive mechanisms. We report here on the multifarious effects of bovine lactoperoxidase (bLPO) on the antagonism between S. gordonii and S. sanguinis versus S. mutans. Some of the effects are apparently counterproductive with respect to maintaining a health-compatible population of streptococci. For example, the bLPO system (comprised of bLPO+SCN−+H2O2) destroys H2O2, thereby abolishing the ability of S. gordonii and S. sanguinis to inhibit the growth of S. mutans. Furthermore, bLPO protein (with or without its substrate) inhibits bacterial growth in a biofilm assay, but sucrose negates the inhibitory effects of the bLPO protein, thereby facilitating adherence of S. mutans in lieu of S. gordonii and S. sanguinis. Our findings may be relevant to environmental pressures that select early supragingival colonizers.
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Nobbs, Angela H., Yongshu Zhang, Ali Khammanivong, and Mark C. Herzberg. "Streptococcus gordonii Hsa Environmentally Constrains Competitive Binding by Streptococcus sanguinis to Saliva-Coated Hydroxyapatite." Journal of Bacteriology 189, no. 8 (February 2, 2007): 3106–14. http://dx.doi.org/10.1128/jb.01535-06.
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ABSTRACT Competition between pioneer colonizing bacteria may determine polymicrobial succession during dental plaque development, but the ecological constraints are poorly understood. For example, more Streptococcus sanguinis than Streptococcus gordonii organisms are consistently isolated from the same intraoral sites, yet S. gordonii fails to be excluded and survives as a species over time. To explain this observation, we hypothesized that S. gordonii could compete with S. sanguinis to adhere to saliva-coated hydroxyapatite (sHA), an in vitro model of the tooth surface. Both species bound similarly to sHA, yet 10- to 50-fold excess S. gordonii DL1 reduced binding of S. sanguinis SK36 by 85 to >95%. S. sanguinis, by contrast, did not significantly compete with S. gordonii to adhere. S. gordonii competed with S. sanguinis more effectively than other species of oral streptococci and depended upon the salivary film on HA. Next, putative S. gordonii adhesins were analyzed for contributions to interspecies competitive binding. Like wild-type S. gordonii, isogenic mutants with mutations in antigen I/II polypeptides (sspAB), amylase-binding proteins (abpAB), and Csh adhesins (cshAB) competed effectively against S. sanguinis. By contrast, an hsa-deficient mutant of S. gordonii showed significantly reduced binding and competitive capabilities, while these properties were restored in an hsa-complemented strain. Thus, Hsa confers a selective advantage to S. gordonii over S. sanguinis in competitive binding to sHA. Hsa expression may, therefore, serve as an environmental constraint against S. sanguinis, enabling S. gordonii to persist within the oral cavity, despite the greater natural prevalence of S. sanguinis in plaque and saliva.
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Woo, Patrick CY, Jade LL Teng, Kit-wah Leung, Susanna KP Lau, Herman Tse, Beatrice HL Wong, and Kwok-yung Yuen. "Streptococcus sinensis may react with Lancefield group F antiserum." Journal of Medical Microbiology 53, no. 11 (November 1, 2004): 1083–88. http://dx.doi.org/10.1099/jmm.0.45745-0.
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Lancefield group F streptococci have been found almost exclusively as members of the ‘Streptococcus milleri’ group, although they have been reported very occasionally in some other streptococcal species. Among 302 patients with bacteraemia caused by viridans streptococci over a 6-year period, three cases were caused by Streptococcus sinensis (type strain HKU4T, HKU5 and HKU6). All three patients had infective endocarditis complicating their underlying chronic rheumatic heart diseases. Gene sequencing showed no base differences between the 16S rRNA gene sequences of HKU5 and HKU6 and that of HKU4T. All three strains were Gram-positive, non-spore-forming cocci arranged in chains. All grew on sheep blood agar as α-haemolytic, grey colonies of 0.5–1 mm in diameter after 24 h incubation at 37 °C in ambient air. Lancefield grouping revealed that HKU5 and HKU6 were Lancefield group F, but HKU4T was non-groupable with Lancefield groups A, B, C, D, F or G antisera. HKU4T was identified by the Vitek system (GPI), API system (20 STREP) and ATB system (ID32 STREP) as 99 % Streptococcus intermedius, 51.3 % S. intermedius and 99.9 % Streptococcus anginosus, respectively. Using the same tests, HKU5 was identified as 87 % Streptococcus sanguinis/Streptococcus gordonii, 59 % Streptococcus salivarius and 99.6 % S. anginosus, respectively, and HKU6 as 87 % S. sanguinis/S. gordonii, 77 % Streptococcus pneumoniae and 98.3 % S. anginosus, respectively. The present data revealed that a proportion of Lancefield group F streptococci could be S. sinensis. Lancefield group F streptococci should not be automatically reported as ‘S. milleri'.
7
Loimaranta, V., N. S. Jakubovics, J. Hytönen, J. Finne, H. F. Jenkinson, and N. Strömberg. "Fluid- or Surface-Phase Human Salivary Scavenger Protein gp340 Exposes Different Bacterial Recognition Properties." Infection and Immunity 73, no. 4 (April 2005): 2245–52. http://dx.doi.org/10.1128/iai.73.4.2245-2252.2005.
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ABSTRACT Salivary scavenger receptor cysteine-rich protein gp340 aggregates streptococci and other bacteria as part of the host innate defense system at mucosal surfaces. In this article, we have investigated the properties of fluid-phase gp340 and hydroxylapatite surface-adsorbed gp340 in aggregation and adherence, respectively, of viridans group streptococci (e.g., Streptococcus gordonii and Streptococcus mutans), non-viridans group streptococci (e.g., Streptococcus pyogenes and Streptococcus suis), and oral Actinomyces. Fluid-phase gp340 and surface-phase gp340 bioforms were differentially recognized by streptococci, which formed three phenotypic groupings according to their modes of interaction with gp340. Group I streptococci were aggregated by and adhered to gp340, and group II streptococci preferentially adhered to surface-bound gp340, while group III streptococci were preferentially aggregated by gp340. Each species of Streptococcus tested was found to contain strains representative of at least two of these gp340 interaction groupings. The gp340 interaction modes I to III and sugar specificities of gp340 binding strains coincided for several species. Many gp340 interactions were sialidase sensitive, and each of the interaction modes (I to III) for S. gordonii was correlated with a variant of sialic acid specificity. Adherence of S. gordonii DL1 (Challis) to surface-bound gp340 was dependent upon expression of the sialic acid binding adhesin Hsa. However, aggregation of cells by fluid-phase gp340 was independent of Hsa and involved SspA and SspB (antigen I/II family) polypeptides. Conversely, both gp340-mediated aggregation and adherence of S. mutans NG8 involved antigen I/II polypeptide. Deletion of the mga virulence regulator gene in S. pyogenes resulted in increased cell aggregation by gp340. These results suggest that salivary gp340 recognizes different bacterial receptors according to whether gp340 is present in the fluid phase or surface bound. This phase-associated differential recognition by gp340 of streptococcal species of different levels of virulence and diverse origins may mediate alternative host responses to commensal or pathogenic bacterial phenotypes.
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Wan, S. X., J. Tian, Y. Liu, A. Dhall, H. Koo, and G. Hwang. "Cross-Kingdom Cell-to-Cell Interactions in Cariogenic Biofilm Initiation." Journal of Dental Research 100, no. 1 (August 27, 2020): 74–81. http://dx.doi.org/10.1177/0022034520950286.
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Candida albicans is known to form polymicrobial biofilms with various Streptococcus spp., including mitis and mutans group streptococci. Streptococcus gordonii (mitis group) has been shown to bind avidly to C. albicans hyphae via direct cell-to-cell interaction, while the cariogenic pathogen Streptococcus mutans (mutans group) interacts with the fungal cells via extracellular glucans. However, the biophysical properties of these cross-kingdom interactions at the single-cell level during the early stage of biofilm formation remain understudied. Here, we examined the binding forces between S. mutans (or S. gordonii) and C. albicans in the presence and absence of in situ glucans on the fungal surface using single-cell atomic force microscopy and their influence on biofilm initiation and subsequent development under cariogenic conditions. The data show that S. gordonii binding force to the C. albicans surface is significantly higher than that of S. mutans to the fungal surface (~2-fold). However, S. mutans binding forces are dramatically enhanced when the C. albicans cell surface is locally coated with extracellular glucans (~6-fold vs. uncoated C. albicans), which vastly exceeds the forces between S. gordonii and C. albicans. The enhanced binding affinity of S. mutans to glucan-coated C. albicans resulted in a larger structure during early biofilm initiation compared to S. gordonii–C. albicans biofilms. Ultimately, this resulted in S. mutans dominance composition in the 3-species biofilm model under cariogenic conditions. This study provides a novel biophysical aspect of Candida-streptococcal interaction whereby extracellular glucans may selectively favor S. mutans binding interactions with C. albicans during cariogenic biofilm development.
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Jakubovics, Nicholas S., Steven R. Gill, Stacey E. Iobst, M. M. Vickerman, and Paul E. Kolenbrander. "Regulation of Gene Expression in a Mixed-Genus Community: Stabilized Arginine Biosynthesis in Streptococcus gordonii by Coaggregation with Actinomyces naeslundii." Journal of Bacteriology 190, no. 10 (March 21, 2008): 3646–57. http://dx.doi.org/10.1128/jb.00088-08.
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ABSTRACT Interactions involving genetically distinct bacteria, for example, between oral streptococci and actinomyces, are central to dental plaque development. A DNA microarray identified Streptococcus gordonii genes regulated in response to coaggregation with Actinomyces naeslundii. The expression of 23 genes changed >3-fold in coaggregates, including that of 9 genes involved in arginine biosynthesis and transport. The capacity of S. gordonii to synthesize arginine was assessed using a chemically defined growth medium. In monoculture, streptococcal arginine biosynthesis was inefficient and streptococci could not grow aerobically at low arginine concentrations. In dual-species cultures containing coaggregates, however, S. gordonii grew to high cell density at low arginine concentrations. Equivalent cocultures without coaggregates showed no growth until coaggregation was evident (9 h). An argH mutant was unable to grow at low arginine concentrations with or without A. naeslundii, indicating that arginine biosynthesis was essential for coaggregation-induced streptococcal growth. Using quantitative reverse transcriptase PCR, the expression of argC, argG, and pyrA b was strongly (10- to 100-fold) up-regulated in S. gordonii monocultures after 3 h of growth when exogenous arginine was depleted. Cocultures without induced coaggregation showed similar regulation. However, within 1 h after coaggregation with A. naeslundii, the expression of argC, argG, and pyrA b in S. gordonii was partially up-regulated although arginine was plentiful, and mRNA levels did not increase further when arginine was diminished. Thus, A. naeslundii stabilizes S. gordonii expression of arginine biosynthesis genes in coaggregates but not cocultures and enables aerobic growth when exogenous arginine is limited.
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Mallaley, P. P., S. A. Halperin, A. Morris, A. MacMillan, and S. F. Lee. "Expression of a pertussis toxin S1 fragment by inducible promoters in oral Streptococcus and the induction of immune responses during oral colonization in mice." Canadian Journal of Microbiology 52, no. 5 (May 1, 2006): 436–44. http://dx.doi.org/10.1139/w05-151.
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Previous work aimed at developing a live oral vaccine expressing pertussis toxin S1 fragment on the surface of the bacterium Streptococcus gordonii elicited a lower than expected antibody response, perhaps because of low antigen expression. In this study, in-frame promoter fusions were constructed to investigate whether an increase in antigen production by the streptococcal vaccine strain results in a better antibody response. The promoters tested were (i) the Streptococcus mutans sucrose-inducible fructosyltransferase (ftf) promoter and (ii) the Bacillus subtilis/Escherichia coli chimeric tetracycline-inducible xyl/tetO promoter. Each of these two promoters was placed upstream of the spaP/s1 fusion gene to drive its expression. The constructs were introduced into S. gordonii DL1 and S. mutans 834. The inducibility of the promoters was confirmed through the determination of SpaP/S1 production via Western blottings. Induced production of SpaP/S1 was observed in S. gordonii and S. mutans with each of the promoters, but the level of expression was the highest in S. mutans, using the xyl/tetO promoter. Thus, S. mutans carrying the xyl/tetO/spaP/s1 construct (S. mutans PM14) was used in oral colonization studies in BALB/c mice. Streptococccus mutans PM14 was able to colonize the animals for the 14-week duration of experimentation. A mucosal IgA response was observed in all the treatment groups but was highest in mice receiving tetracycline induction. In the mouse model of Bordetella pertussis respiratory infection, animals colonized with S. mutans PM14 showed a decreased in B. pertussis lung colony count (P = 0.03) on day 3 compared with control mice colonized by the parent S. mutans 834.Key words: pertussis, Streptococcus mutans, Streptococcus gordonii, oral colonization.
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W S Harty, Derek. "Virulence factors in streptococcal infective endocarditis." Microbiology Australia 26, no. 3 (2005): 114. http://dx.doi.org/10.1071/ma05114.
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Infective endocarditis (IE) is a life threatening, endovascular infection occurring when bacteria enter the blood stream and adhere to heart valves. Mortality rates remain in the range of 11-27%. The most common infecting micro-organisms are now the staphylococci (44%) although streptococci (31%) and particularly the oral streptococci (21%) are still major causative agents. Many different oral streptococci have been isolated from IE cases, the most common being Streptococcus sanguinis, Streptococcus oralis, Streptococcus gordonii, Streptococcus mitis, Streptococcus anginosus group and mutans streptococci.
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Xu, Yifan, Andreas Itzek, and Jens Kreth. "Comparison of genes required for H2O2 resistance in Streptococcus gordonii and Streptococcus sanguinis." Microbiology 160, no. 12 (December 1, 2014): 2627–38. http://dx.doi.org/10.1099/mic.0.082156-0.
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Hydrogen peroxide (H2O2) is produced by several members of the genus Streptococcus mainly through the pyruvate oxidase SpxB under aerobic growth conditions. The acute toxic nature of H2O2 raises the interesting question of how streptococci cope with intrinsically produced H2O2, which subsequently accumulates in the microenvironment and threatens the closely surrounding population. Here, we investigate the H2O2 susceptibility of oral Streptococcus gordonii and Streptococcus sanguinis and elucidate potential mechanisms of how they protect themselves from the deleterious effect of H2O2. Both organisms are considered primary colonizers and occupy the same intraoral niche making them potential targets for H2O2 produced by other species. We demonstrate that S. gordonii produces relatively more H2O2 and has a greater ability for resistance to H2O2 stress. Functional studies show that, unlike in Streptococcus pneumoniae, H2O2 resistance is not dependent on a functional SpxB and confirms the important role of the ferritin-like DNA-binding protein Dps. However, the observed increased H2O2 resistance of S. gordonii over S. sanguinis is likely to be caused by an oxidative stress protection machinery present even under anaerobic conditions, while S. sanguinis requires a longer period of time for adaptation. The ability to produce more H2O2 and be more resistant to H2O2 might aid S. gordonii in the competitive oral biofilm environment, since it is lower in abundance yet manages to survive quite efficiently in the oral biofilm.
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Aspiras, Marcelo B., Karen M. Kazmerzak, Paul E. Kolenbrander, Roderick McNab, Neil Hardegen, and Howard F. Jenkinson. "Expression of Green Fluorescent Protein in Streptococcus gordonii DL1 and Its Use as a Species-Specific Marker in Coadhesion with Streptococcus oralis 34 in Saliva-Conditioned Biofilms In Vitro." Applied and Environmental Microbiology 66, no. 9 (September 1, 2000): 4074–83. http://dx.doi.org/10.1128/aem.66.9.4074-4083.2000.
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ABSTRACT Streptococcus gordonii is one of the predominant streptococci in the biofilm ecology of the oral cavity. It interacts with other bacteria through receptor-adhesin complexes formed between cognate molecules on the surfaces of the partner cells. To study the spatial organization of S. gordonii DL1 in oral biofilms, we used green fluorescent protein (GFP) as a species-specific marker to identify S. gordonii in a two-species in vitro oral biofilm flowcell system. To drive expression of gfp, we isolated and characterized an endogenous S. gordonii promoter,PhppA, which is situated upstream of the chromosomalhppA gene encoding an oligopeptide-binding lipoprotein. A chromosomal chloramphenicol acetyltransferase (cat) gene fusion with PhppA was constructed and used to demonstrate that PhppA was highly active throughout the growth of bacteria in batch culture. A promoterless 0.8-kb gfp(′gfp) cassette was PCR amplified from pBJ169 and subcloned to replace the cat cassette downstream of the S. gordonii-derived PhppA in pMH109-HPP, generating pMA1. Subsequently, the PhppA-′gfp cassette was PCR amplified from pMA1 and subcloned into pDL277 and pVA838 to generate the Escherichia coli-S. gordonii shuttle vectors pMA2 and pMA3, respectively. Each vector was transformed into S. gordonii DL1 aerobically to ensure GFP expression. Flow cytometric analyses of aerobically grown transformant cultures were performed over a 24-h period, and results showed that GFP could be successfully expressed in S. gordonii DL1 fromPhppA and that S. gordonii DL1 transformed with the PhppA-′gfp fusion plasmid stably maintained the fluorescent phenotype. Fluorescent S. gordonii DL1 transformants were used to elucidate the spatial arrangement ofS. gordonii DL1 alone in biofilms or with the coadhesion partner Streptococcus oralis 34 in two-species biofilms in a saliva-conditioned in vitro flowcell system. These results show for the first time that GFP expression in oral streptococci can be used as a species-specific marker in model oral biofilms.
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Urano-Tashiro, Yumiko, Keitarou Saiki, Yuki Yamanaka, Yuiko Ishikawa, and Yukihiro Takahashi. "Streptococcus gordonii DL1 evades polymorphonuclear leukocyte-mediated killing via resistance to lysozyme." PLOS ONE 16, no. 12 (December 20, 2021): e0261568. http://dx.doi.org/10.1371/journal.pone.0261568.
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Streptococcus gordonii is an etiological bacterial agent of infective endocarditis. Although the pathogenesis mechanisms are not well understood, the interaction between streptococci and phagocytes is considered important for the development of infective endocarditis. Previous studies show that some S. gordonii strains, including DL1, survive in polymorphonuclear leukocytes (PMNs), whereas other strains such as SK12 are sensitive to PMN-dependent killing. In this study, we assessed the differences between the sensitivity of S. gordonii DL1 and S. gordonii SK12 to PMN-dependent killing. S. gordonii DL1 showed a higher survival when treated with PMNs than SK12. Both S. gordonii DL1 and S. gordonii SK12 showed high resistance to low pH condition. Compared to S. gordonii SK12, S. gordonii DL1 was sensitive to hydrogen peroxide. However, the resistance of S. gordonii DL1 to the tested bactericidal agents, especially lysozyme, was higher than that of SK12. Furthermore, we performed a bactericidal assay by treating a mixture of S. gordonii DL1 and SK12 with PMNs. S. gordonii DL1 did not enhance the survival of S. gordonii SK12 exposed to PMNs. These results indicated that S. gordonii DL1 is resistant to bactericidal agents that degrade bacteria in phagolysosomes. In addition, there was no secretory factor involved in the resistance to bactericidal agents. The findings of this study may help develop treatments for infective endocarditis caused by S. gordonii.
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Wang, Bing-Yan, and Howard K. Kuramitsu. "Interactions between Oral Bacteria: Inhibition of Streptococcus mutans Bacteriocin Production by Streptococcus gordonii." Applied and Environmental Microbiology 71, no. 1 (January 2005): 354–62. http://dx.doi.org/10.1128/aem.71.1.354-362.2005.
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ABSTRACT Streptococcus mutans has been recognized as an important etiological agent in human dental caries. Some strains of S. mutans also produce bacteriocins. In this study, we sought to demonstrate that bacteriocin production by S. mutans strains GS5 and BM71 was mediated by quorum sensing, which is dependent on a competence-stimulating peptide (CSP) signaling system encoded by the com genes. We also demonstrated that interactions with some other oral streptococci interfered with S. mutans bacteriocin production both in broth and in biofilms. The inhibition of S. mutans bacteriocin production by oral bacteria was stronger in biofilms than in broth. Using transposon Tn916 mutagenesis, we identified a gene (sgc; named for Streptococcus gordonii challisin) responsible for the inhibition of S. mutans bacteriocin production by S. gordonii Challis. Interruption of the sgc gene in S. gordonii Challis resulted in attenuated inhibition of S. mutans bacteriocin production. The supernatant fluids from the sgc mutant did not inactivate the exogenous S. mutans CSP as did those from the parent strain Challis. S. gordonii Challis did not inactivate bacteriocin produced by S. mutans GS5. Because S. mutans uses quorum sensing to regulate virulence, strategies designed to interfere with these signaling systems may have broad applicability for biological control of this caries-causing organism.
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Jakubovics, Nicholas S., Steven W. Kerrigan, Angela H. Nobbs, Nicklas Strömberg, Craig J. van Dolleweerd, Dermot M. Cox, Charles G. Kelly, and Howard F. Jenkinson. "Functions of Cell Surface-Anchored Antigen I/II Family and Hsa Polypeptides in Interactions of Streptococcus gordonii with Host Receptors." Infection and Immunity 73, no. 10 (October 2005): 6629–38. http://dx.doi.org/10.1128/iai.73.10.6629-6638.2005.
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ABSTRACT Streptococcus gordonii colonizes multiple sites within the human oral cavity. This colonization depends upon the initial interactions of streptococcal adhesins with host receptors. The adhesins that bind salivary agglutinin glycoprotein (gp340) and human cell surface receptors include the antigen I/II (AgI/II) family polypeptides SspA and SspB and a sialic acid-binding surface protein designated Hsa or GspB. In this study we determined the relative functions of the AgI/II polypeptides and Hsa in interactions of S. gordonii DL1 (Challis) with host receptors. For an isogenic mutant with the sspA and sspB genes deleted the levels of adhesion to surface-immobilized gp340 were reduced 40%, while deletion of the hsa gene alone resulted in >80% inhibition of bacterial cell adhesion to gp340. Adhesion of S. gordonii DL1 cells to gp340 was sialidase sensitive, verifying that Hsa has a major role in mediating sialic acid-specific adhesion to gp340. Conversely, aggregation of S. gordonii cells by fluid-phase gp340 was not affected by deletion of hsa but was eliminated by deletion of the sspA and sspB genes. Deletion of the AgI/II polypeptide genes had no measurable effect on hsa mRNA levels or Hsa surface protein expression, and deletion of hsa did not affect AgI/II polypeptide expression. Further analysis of mutant phenotypes showed that the Hsa and AgI/II proteins mediated adhesion of S. gordonii DL1 to human HEp-2 epithelial cells. Hsa was also a principal streptococcal cell surface component promoting adhesion of human platelets to immobilized streptococci, but Hsa and AgI/II polypeptides acted in concert in mediating streptococcal cell-platelet aggregation. The results suggest that Hsa directs primary adhesion events for S. gordonii DL1 (Challis) with immobilized gp340, epithelial cells, and platelets. AgI/II polypeptides direct gp340-mediated aggregation, facilitate multimodal interactions necessary for platelet aggregation, and modulate S. gordonii-host engagements into biologically productive phenomena.
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Huang, Xuelian, Christopher M. Browngardt, Min Jiang, Sang-Joon Ahn, Robert A. Burne, and Marcelle M. Nascimento. "Diversity in Antagonistic Interactions between Commensal Oral Streptococci and Streptococcus mutans." Caries Research 52, no. 1-2 (December 20, 2017): 88–101. http://dx.doi.org/10.1159/000479091.
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Arginine metabolism via the arginine deiminase system (ADS) of oral bacteria generates ammonia, which can increase the pH of oral biofilms and decrease the risk for dental caries. Antagonistic interactions between ADS-positive and cariogenic bacteria in oral biofilms may be an important ecological determinant of caries. This study investigated the antagonistic potential and mechanisms of clinical isolates of arginolytic streptococci on and by Streptococcus mutans UA159, a well-characterized cariogenic human isolate. Low-passage isolates of Streptococcus gordonii, Streptococcus sanguinis, Streptococcus parasanguinis, Streptococcus australis, and Streptococcus cristatus inhibited the growth of S. mutans to various degrees when they were inoculated on growth media first or simultaneously with S. mutans. The antagonistic effects of arginolytic strains against S. mutans and the production of H2O2 by these strains were enhanced during growth in a less-rich medium or when galactose was substituted for glucose as the primary carbohydrate source. Pyruvate oxidase was the dominant pathway for H2O2 production by arginolytic strains, but lactate oxidase activity was also detected in some strains of S. gordonii and S. cristatus. UA159 inhibited the growth of all tested arginolytic strains when inoculated first, especially in aerobic conditions. However, the antagonistic effects of S. mutans on certain strains of S. gordonii and S. australis were not observed during anaerobic growth in the presence of arginine. Thus, arginolytic commensal streptococci may have a synergistically positive impact on the ecology of oral biofilms by moderating biofilm pH while antagonizing the growth and virulence of caries pathogens.
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Chalmers, Natalia I., Robert J. Palmer, John O. Cisar, and Paul E. Kolenbrander. "Characterization of a Streptococcus sp.-Veillonella sp. Community Micromanipulated from Dental Plaque." Journal of Bacteriology 190, no. 24 (September 19, 2008): 8145–54. http://dx.doi.org/10.1128/jb.00983-08.
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ABSTRACT Streptococci and veillonellae occur in mixed-species colonies during formation of early dental plaque. One factor hypothesized to be important in assembly of these initial communities is coaggregation (cell-cell recognition by genetically distinct bacteria). Intrageneric coaggregation of streptococci occurs when a lectin-like adhesin on one streptococcal species recognizes a receptor polysaccharide (RPS) on the partner species. Veillonellae also coaggregate with streptococci. These genera interact metabolically; lactic acid produced by streptococci is a carbon source for veillonellae. To transpose these interactions from undisturbed dental plaque to an experimentally tractable in vitro biofilm model, a community consisting of RPS-bearing streptococci juxtaposed with veillonellae was targeted by quantum dot-based immunofluorescence and then micromanipulated off the enamel surface and cultured. Besides the expected antibody-reactive cell types, a non-antibody-reactive streptococcus invisible during micromanipulation was obtained. The streptococci were identified as Streptococcus oralis (RPS bearing) and Streptococcus gordonii (adhesin bearing). The veillonellae could not be cultivated; however, a veillonella 16S rRNA gene sequence was amplified from the original isolation mixture, and this sequence was identical to the sequence of the previously studied organism Veillonella sp. strain PK1910, an oral isolate in our culture collection. S. oralis coaggregated with S. gordonii by an RPS-dependent mechanism, and both streptococci coaggregated with PK1910, which was used as a surrogate during in vitro community reconstruction. The streptococci and strain PK1910 formed interdigitated three-species clusters when grown as a biofilm using saliva as the nutritional source. PK1910 grew only when streptococci were present. This study confirms that RPS-mediated intrageneric coaggregation occurs in the earliest stages of plaque formation by bringing bacteria together to create a functional community.
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Drobni, Mirva, Tong Li, Carina Krüger, Vuokko Loimaranta, Mogens Kilian, Lennart Hammarström, Hans Jörnvall, Tomas Bergman, and Nicklas Strömberg. "Host-Derived Pentapeptide Affecting Adhesion, Proliferation, and Local pH in Biofilm Communities Composed of Streptococcus and Actinomyces Species." Infection and Immunity 74, no. 11 (August 28, 2006): 6293–99. http://dx.doi.org/10.1128/iai.00068-06.
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ABSTRACT Salivary proline-rich proteins (PRPs) attach commensal Actinomyces and Streptococcus species to teeth. Here, gel filtration, mass spectrometry and Edman degradation were applied to show the release of a pentapeptide, RGRPQ, from PRP-1 upon proteolysis by Streptococcus gordonii. Moreover, synthetic RGRPQ and derivatives were used to investigate associated innate properties and responsible motifs. The RGRPQ peptide increased 2.5-fold the growth rate of S. gordonii via a Q-dependent sequence motif and selectively stimulated oral colonization of this organism in a rat model in vivo. In contrast, the growth of Streptococcus mutans, implicated in caries, was not affected. While the entire RGRPQ sequence was required to block sucrose-induced pH-decrease by S. gordonii and S. mutans, the N-terminal Arg residue mediated the pH increase (i.e., ammonia production) by S. gordonii alone (which exhibits Arg catabolism to ammonia). Strains of commensal viridans streptococci exhibited PRP degradation and Arg catabolism, whereas cariogenic species did not. The RGRPQ peptide mediated via a differential Q-dependent sequence motif, adhesion inhibition, and desorption of PRP-1-binding strains of A. naeslundii genospecies 2 (5 of 10 strains) but not of S. gordonii (n = 5). The inhibitable A. naeslundii strains alone displayed the same binding profile as S. gordonii to hybrid peptides terminating in RGRPQ or GQSPQ, derived from the middle or C-terminal segments of PRP-1. The present findings indicate the presence of a host-bacterium interaction in which a host peptide released by bacterial proteolysis affects key properties in biofilm formation.
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Zhang, Michael, Lifang Yan, Guan Zhu, Michael Holifield, Donna Todd, and Shuping Zhang. "Streptococcus troglodytidis sp. nov., isolated from a foot abscess of a chimpanzee (Pan troglodytes)." International Journal of Systematic and Evolutionary Microbiology 63, Pt_2 (February 1, 2013): 449–53. http://dx.doi.org/10.1099/ijs.0.038133-0.
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A facultative anaerobic, non-motile, non-spore-forming, Gram-positive-staining, coccus-shaped bacterium was isolated from an abscess on the right foot of a chimpanzee (Pan troglodytes). The colonies were β-haemolytic. Catalase and oxidase activities were negative. The Lancefield group B antigen was expressed. On the basis of morphological and biochemical characteristics, the bacterium was tentatively identified as a streptococcal species. 16S rRNA gene sequence analysis indicated that the bacterium shared 96.7 %, 96.4 %, 96.1 %, 95.8 % and 95.7 % sequence similarities with Streptococcus gordonii , S. cristatus , S. intermedius , S. anginosus and S. constellatus , respectively. Phylogenetic analyses based on the sequences of the 16S rRNA gene and housekeeping genes encoding d-alanine : d-alanine ligase (ddl), the β-subunit of RNA polymerase (rpoB) and manganese-dependent superoxide dismutase (sodA) revealed that the bacterium represented a novel species closely related to, albeit different from, S. gordonii , S. cristatus and the anginosus streptococci. The name Streptococcus troglodytidis sp. nov. is proposed. The type strain is M09-11185T ( = ATCC BAA-2337T = KCTC 33006T).
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Egland, Paul G., Laurence D. Dû, and Paul E. Kolenbrander. "Identification of Independent Streptococcus gordonii SspA and SspB Functions in Coaggregation withActinomyces naeslundii." Infection and Immunity 69, no. 12 (December 1, 2001): 7512–16. http://dx.doi.org/10.1128/iai.69.12.7512-7516.2001.
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ABSTRACT The initial stages of dental plaque formation involve the adherence of early colonizing organisms such as Streptococcus gordonii and Actinomyces naeslundii to the saliva-coated tooth surface and to each other. The S. gordonii surface proteins SspA and SspB are known to play a role in adherence to salivary proteins and mediate coaggregation with other bacteria. Coaggregation is the adhesin receptor-mediated interaction between genetically distinct cell types and appears to be ubiquitous among oral isolates. To define the function of SspA and SspB separately on the surface of their natural host, we constructed and analyzed the coaggregation properties of an isogenicsspB mutant of S. gordonii DL1, ansspAB double mutant, and a previously describedsspA mutant. A. naeslundii strains have been previously classified into six coaggregation groups based on the nature of their coaggregations with S. gordonii DL1 and other oral streptococci. Coaggregation assays with thesspA and sspB mutants showed that SspA and SspB are the streptococcal proteins primarily responsible for defining these coaggregation groups and, thus, are highly significant in the establishment of early dental plaque. SspA exhibited two coaggregation-specific functions. It participated in lactose-inhibitable and -noninhibitable interactions, while SspB mediated only lactose-noninhibitable coaggregations. Accordingly, thesspAB double mutant lacked these functions and allowed us to detect a third coaggregation interaction with one of these organisms. These proteins may play an important role in development ofS. gordonii-A. naeslundii communities in early dental plaque. Understanding these adhesin proteins will aid investigations of complex microbial communities that characterize periodontal diseases.
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Bamford, Caroline V., Anita d'Mello, Angela H. Nobbs, Lindsay C. Dutton, M. Margaret Vickerman, and Howard F. Jenkinson. "Streptococcus gordonii Modulates Candida albicans Biofilm Formation through Intergeneric Communication." Infection and Immunity 77, no. 9 (June 15, 2009): 3696–704. http://dx.doi.org/10.1128/iai.00438-09.
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ABSTRACT The fungus Candida albicans colonizes human oral cavity surfaces in conjunction with a complex microflora. C. albicans SC5314 formed biofilms on saliva-coated surfaces that in early stages of development consisted of ∼30% hyphal forms. In mixed biofilms with the oral bacterium Streptococcus gordonii DL1, hyphal development by C. albicans was enhanced so that biofilms consisted of ∼60% hyphal forms. Cell-cell contact between S. gordonii and C. albicans involved Streptococcus cell wall-anchored proteins SspA and SspB (antigen I/II family polypeptides). Repression of C. albicans hyphal filament and biofilm production by the quorum-sensing molecule farnesol was relieved by S. gordonii. The ability of a luxS mutant of S. gordonii deficient in production of autoinducer 2 to induce C. albicans hyphal formation was reduced, and this mutant suppressed farnesol inhibition of hyphal formation less effectively. Coincubation of the two microbial species led to activation of C. albicans mitogen-activated protein kinase Cek1p, inhibition of Mkc1p activation by H2O2, and enhanced activation of Hog1p by farnesol, which were direct effects of streptococci on morphogenetic signaling. These results suggest that interactions between C. albicans and S. gordonii involve physical (adherence) and chemical (diffusible) signals that influence the development of biofilm communities. Thus, bacteria may play a significant role in modulating Candida carriage and infection processes in the oral cavity.
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Kerrigan, Steven W., Nick S. Jakubouvics, Gerardene Meade, Howard F. Jenkinson, and Dermot M. Cox. "A Novel GPIbα Binding Protein on Streptococcus Gordonii Induces Platelet Rolling at Low Shear." Blood 104, no. 11 (November 16, 2004): 3663. http://dx.doi.org/10.1182/blood.v104.11.3663.3663.
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Abstract Infective endocarditis is associated with considerable morbidity and mortality and oral Streptococci are the priniciple causative organism. Platelet adhesion and subsequent aggregation play a critical role in the pathogenesis and dissemination of the infective process. The mechanism by which S. gordonii interacts with and subsequently leads to platelet activation is currently unknown. Previously we described the ability of Streptococcus sanguis to induce platelet aggregation via the platelet vonWillebrand factor receptor, GPIbα, however identification of the bacterial protein involved was not established. Here we describe the novel interaction between a Streptococcal protein that triggers aggregation via platelet GPIbα, in a unique fashion. Wildtype S. sanguis (133–79) and S. gordonii (DL1) support platelet adhesion and induce αIIbβ3 dependent platelet aggregation. Pre-incubation of platelets with an anti-GPIbα antibody inhibited the adhesion (61±6%, p<0.001) and abolished platelet aggregation (0% of control, p<0.001) induced by S. gordonii. These results suggest that GPIbα is a key receptor for recognition of platelets by streptococci. Passing a mutanolysin cell wall extract of S. sanguis through a GPIb affinity column identified a highly glycosylated protein, Hsa, also present on S. gordonii. S. gordonii DL-1 deficient in the Hsa gene, was generated by allelic exchange with an antibiotic resistance cassette. Platelet adhesion to S. gordonii ΔHsa was reduced by 41±5%, (p<0.001), however aggregation was unaffected (49±7% vs 55±5% wt). To confirm that Hsa was binding to platelet GPIbα we immobilised soluble GPIbα (glycocalicin, 0.2μg/ml) on a 96 well plate. Wildtype S. gordonii bound to immobilised glycocalicin, however, the Hsa mutant adhered significantly less (9±3% of wildtype, p<0.001). Furthermore, wildtype S. gordonii induced αIIbβ3 dependent platelet aggregation in washed platelets in the absence of vWf, suggesting a direct interaction between Hsa and GPIbα. We further investigated the interaction between GPIbα and Hsa under shear. Experiments were recorded in real time for a period of 8 minutes. Upon commencement of shear (50s-1), platelets interacted with S. gordonii DL-1 with a rolling fashion followed by firm adhesion. This adhesion was completely inhibited by addition of an anti-GPIbα antibody. When platelets were sheared over immobilized S. gordonii ΔHsa no interaction was observed. In addition, S. gordonii DL-1 failed to interact with platelets at the higher shear rate of 500s-1. Collectively, these results identify a unique interaction between S. gordonii Hsa and platelet GPIbα. This interaction occurs at static and low shear but not at high shear, which is in direct contrast to the interaction between vwf and GPIbα. Furthermore, we propose that the platelet interaction with S. gordonii appears to be a 2 step process. Firstly, platelets roll across the S. gordonii via a GPIbα - Hsa interaction. Following this a second more stable interaction firmly immobilizes the platelet, thereby facilitating the intravascular colonization of a septic plaque.
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Jakubovics, Nicholas S., Jane L. Brittan, Lindsay C. Dutton, and Howard F. Jenkinson. "Multiple adhesin proteins on the cell surface of Streptococcus gordonii are involved in adhesion to human fibronectin." Microbiology 155, no. 11 (November 1, 2009): 3572–80. http://dx.doi.org/10.1099/mic.0.032078-0.
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Adhesion of bacterial cells to fibronectin (FN) is thought to be a pivotal step in the pathogenesis of invasive infectious diseases. Viridans group streptococci such as Streptococcus gordonii are considered commensal members of the oral microflora, but are important pathogens in infective endocarditis. S. gordonii expresses a battery of cell-surface adhesins that act alone or in concert to bind host receptors. Here, we employed molecular genetic approaches to determine the relative contributions of five known S. gordonii surface proteins to adherence to human FN. Binding levels to FN by isogenic mutants lacking Hsa glycoprotein were reduced by 70 %, while mutants lacking CshA and CshB fibrillar proteins showed approximately 30 % reduced binding. By contrast, disruption of antigen I/II adhesin genes sspA and sspB in a wild-type background did not result in reduced FN binding. Enzymic removal of sialic acids from FN led to reduced S. gordonii DL1 adhesion (>50 %), but did not affect binding by the hsa mutant, indicating that Hsa interacts with sialic acid moieties on FN. Conversely, desialylation of FN did not affect adherence levels of Lactococcus lactis cells expressing SspA or SspB polypeptides. Complementation of the hsa mutant partially restored adhesion to FN. A model is proposed for FN binding by S. gordonii in which Hsa and CshA/CshB are primary adhesins, and SspA or SspB play secondary roles. Understanding the basis of oral streptococcal interactions with FN will provide a foundation for development of new strategies to control infective endocarditis.
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Love, Robert M., Malcolm D. McMillan, Yoonsuk Park, and Howard F. Jenkinson. "Coinvasion of Dentinal Tubules byPorphyromonas gingivalis and Streptococcus gordonii Depends upon Binding Specificity of Streptococcal Antigen I/II Adhesin." Infection and Immunity 68, no. 3 (March 1, 2000): 1359–65. http://dx.doi.org/10.1128/iai.68.3.1359-1365.2000.
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ABSTRACT Cell wall-anchored polypeptides of the antigen I/II family are produced by many species of oral streptococci. These proteins mediate adhesion of streptococci to salivary glycoproteins and to other oral microorganisms and promote binding of cells to collagen type I and invasion of dentinal tubules. Since infections of the root canal system have a mixed anaerobic bacterial etiology, we investigated the hypothesis that coadhesion of anaerobic bacteria with streptococci may facilitate invasive endodontic disease. Porphyromonas gingivalis ATCC 33277 cells were able to invade dentinal tubules when cocultured with Streptococcus gordonii DL1 (Challis) but not when cocultured with Streptococcus mutans NG8. An isogenic noninvasive mutant of S. gordonii, with production of SspA and SspB (antigen I/II family) polypeptides abrogated, was deficient in binding to collagen and had a 40% reduced ability to support adhesion of P. gingivalis. Heterologous expression of the S. mutans SpaP (antigen I/II) protein in this mutant restored collagen binding and tubule invasion but not adhesion toP. gingivalis or the ability to promote P. gingivalis coinvasion of dentin. An isogenic afimbrial mutant ofP. gingivalis had 50% reduced binding to S. gordonii cells but was unaffected in the ability to coinvade dentinal tubules with S. gordonii wild-type cells. Expression of the S. gordonii SspA or SspB polypeptide on the surface of Lactococcus lactis cells endowed these bacteria with the abilities to bind P. gingivalis, penetrate dentinal tubules, and promote P. gingivaliscoinvasion of dentin. The results demonstrate that collagen-binding andP. gingivalis-binding properties of antigen I/II polypeptides are discrete functions. Specificity of antigen I/II polypeptide recognition accounts for the ability of P. gingivalis to coinvade dentinal tubules with S. gordonii but not with S. mutans. This provides evidence that the specificity of interbacterial coadhesion may influence directly the etiology of pulpal and periapical diseases.
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Al-Ahmad, Ali, Thorsten Mathias Auschill, Gabriele Braun, Elmar Hellwig, and Nicole Birgit Arweiler. "Overestimation of Streptococcus mutans prevalence by nested PCR detection of the 16S rRNA gene." Journal of Medical Microbiology 55, no. 1 (January 1, 2006): 109–13. http://dx.doi.org/10.1099/jmm.0.46280-0.
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This study was carried out in order to compare two PCR-based methods in the detection of Streptococcus mutans. The first PCR method was based on primers for the 16S rRNA gene and the second method was based on specific primers that targeted the glucosyltransferase gene (gtfB). Each PCR was performed with eight different streptococci from the viridans group, five other streptococci and 17 different non-streptococcal bacterial strains. Direct use of the S. mutans 16S rRNA gene-specific primers revealed that Streptococcus gordonii and Streptococcus infantis were also detected. After amplifying the 16S rRNA gene with universal primers and subsequently performing nested PCR, the S. mutans-specific nested primers based on the 16S rRNA gene detected all tested streptococci. There was no cross-reaction of the gtfB primers after direct PCR. Our results indicate that direct PCR and nested PCR based on 16S rRNA genes can reveal false-positive results for oral streptococci and lead to an overestimation of the prevalence of S. mutans with regards to its role as the most prevalent causative agent of dental caries.
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Karaaslan, Fatih, Turgut Demir, and Ozlem Barış. "Effect of Periodontal Disease-associated Bacteria on the Formation of Dental Calculus: An In Vitro Study." Journal of Advanced Oral Research 11, no. 2 (April 25, 2020): 165–71. http://dx.doi.org/10.1177/2320206820919591.
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Aim: To investigate whether bacteria that play a major role in periodontal disease pathology and in the formation of dental plaque also affect the formation of dental calculus, which is a predisposing factor for the initiation and progression of periodontal diseases. Materials and Methods: This was an in vitro study, and cultures of bacteria were obtained from the American Type Culture Collection and Department of Biology, Faculty of Science, Atatürk University. Young cultures of bacteria of Streptococcus mutans ( S. mutans), Streptococcus sanguinis ( S. sanguinis), Streptococcus gordonii ( S. gordonii), Aggregatibacter actinomycetemcomitans ( A. actinomycetemcomitans), Porphyromonas gingivalis ( P. gingivalis), Fusobacterium nucleatum ( F. nucleatum), and Corynebacterium matruchotii ( C. matruchotii) were prepared in media containing their specific enriching factors. B2 solid, B4 solid, and B2 liquid media were used to determine active calcification, whereas the mineral salt basal (MSB) medium was used to observe passive calcification. Calcification in the media was measured under light microscopy and in MSB using a spectrophotometer and was recorded as the percent transmittance. Results: S. mutans, S. sanguinis, and S. gordonii showed calcification in the B2 medium. S. mutans, S. sanguinis, S. gordonii, and C. matruchotii demonstrated calcification in MSB. A. actinomycetemcomitans, P. gingivalis, and F. nucleatum did not show any calcification. Conclusions: It was concluded that streptococci present in dental plaque take part in the formation of dental calculus, whereas periodontopathogens have no role in the formation of dental calculus.
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Fujiki, Jumpei, Shin-ichi Yoshida, Tomohiro Nakamura, Keisuke Nakamura, Yurika Amano, Keita Nishida, Keitaro Nishi, et al. "Novel Virulent Bacteriophage ΦSG005, Which Infects Streptococcus gordonii, Forms a Distinct Clade among Streptococcus Viruses." Viruses 13, no. 10 (September 29, 2021): 1964. http://dx.doi.org/10.3390/v13101964.
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Bacteriophages are viruses that specifically infect bacteria and are classified as either virulent phages or temperate phages. Despite virulent phages being promising antimicrobial agents due to their bactericidal effects, the implementation of phage therapy depends on the availability of virulent phages against target bacteria. Notably, virulent phages of Streptococcus gordonii, which resides in the oral cavity and is an opportunistic pathogen that can cause periodontitis and endocarditis have previously never been found. We thus attempted to isolate virulent phages against S. gordonii. In the present study, we report for the first time a virulent bacteriophage against S. gordonii, ΦSG005, discovered from drainage water. ΦSG005 is composed of a short, non-contractile tail and a long head, revealing Podoviridae characteristics via electron microscopic analysis. In turbidity reduction assays, ΦSG005 showed efficient bactericidal effects on S. gordonii. Whole-genome sequencing showed that the virus has a DNA genome of 16,127 bp with 21 coding sequences. We identified no prophage-related elements such as integrase in the ΦSG005 genome, demonstrating that the virus is a virulent phage. Phylogenetic analysis indicated that ΦSG005 forms a distinct clade among the streptococcus viruses and is positioned next to streptococcus virus C1. Molecular characterization revealed the presence of an anti-CRISPR (Acr) IIA5-like protein in the ΦSG005 genome. These findings facilitate our understanding of streptococcus viruses and advance the development of phage therapy against S. gordonii infection.
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Hamada, Tomoyuki, Masatsugu Kawashima, Haruo Watanabe, Junji Tagami, and Hidenobu Senpuku. "Molecular Interactions of Surface Protein Peptides of Streptococcus gordonii with Human Salivary Components." Infection and Immunity 72, no. 8 (August 2004): 4819–26. http://dx.doi.org/10.1128/iai.72.8.4819-4826.2004.
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ABSTRACT Oral streptococci play a large role in dental biofilm formation, and several types interact as early colonizers with the enamel salivary pellicle to form the primary biofilm, as well as to incorporate other bacteria on tooth surfaces. Interactions of surface molecules of individual streptococci with the salivary pellicle on the tooth surface have an influence on the etiological properties of an oral biofilm. To elucidate the molecular interactions of streptococci with salivary components, binding between surface protein (SspB and PAg) peptides of Streptococcus gordonii and Streptococcus sobrinus were investigated by utilizing BIAcore biosensor technology. The analogous peptide [change of T at position 400 to K in SspB(390-402), resulting in the SspB(390-T400K-402) peptide] from S. gordonii showed the greatest response for binding to salivary components and inhibited the binding of Streptococcus sanguis by more than 50% in a competitive inhibition assay in a comparison with other SspB and PAg peptides. This peptide also bound to the high-molecular-weight protein complex of salivary components and the agglutinin (gp340/DMBT1) peptide (scavenger receptor cysteine-rich domain peptide 2 [SRCRP 2]). In addition, the SspB(390-T400K-402) peptide was visualized by two surface positive charges in connection with the positively charged residues, in which lysine was a key residue for binding. Therefore, the region containing lysine may have binding activity in S. gordonii and S. sanguis, and the SRCRP 2 region may function as a receptor for the binding. These findings may provide useful information regarding the molecular mechanism of early biofilm formation by streptococci on tooth surfaces.
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Grönroos, L., M. Saarela, J. Mättö, U. Tanner-Salo, A. Vuorela, and S. Alaluusua. "Mutacin Production by Streptococcus mutans May Promote Transmission of Bacteria from Mother to Child." Infection and Immunity 66, no. 6 (June 1, 1998): 2595–600. http://dx.doi.org/10.1128/iai.66.6.2595-2600.1998.
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ABSTRACT The production of bacteriocin-like inhibitory substances, mutacins, by mutans streptococci varies among isolates. To find if the degree of mutacin activity of an isolate was related to its transmission between mother and her child, 19 mothers and their 18-month- to 3-year-old children were sampled for their oral mutans streptococci. In addition, the stability of mutacin activity was studied with isolates from the mothers and with isolates from five unrelated 5-year-old children in 5- to 7-year follow-up studies. A total of 145 oral mutans streptococcal isolates were serotyped by immunodiffusion, ribotyped, and mutacin typed by the stab culture technique. Mutacin was produced by 88% of the strains against more than 1 of the 14 indicator strains, representing mutans streptococci,Streptococcus sanguis, Streptococcus salivarius, Streptococcus oralis, Streptococcus gordonii, and Streptococcus pyogenes. Streptococcus mutans isolates showed more inhibitory activity than didStreptococcus sobrinus isolates. Identical ribotypes had similar mutacin activity profiles within a subject, initially and in the follow-up studies, in all but two cases. The mothers harbored a total of 37 different mutans streptococcal ribotypes. Six children were negative for mutans streptococci. Transmission was probable in 9 of 20 mother-child pairs on the basis of the presence of identical strains, as determined by ribotyping and bacteriocin (mutacin) typing. S. mutansstrains shared between a mother and her child showed a broader spectrum of inhibitory activity than did nontransmitted strains. In conclusion, the mutacin activity of clinical isolates is reasonably stable, and this virulence factor seems to be of clinical importance in early colonization by S. mutans.
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Warren, Travis K., S. Amanda Lund, Kevin F. Jones, and Dennis E. Hruby. "Comparison of transformation protocols in Streptococcus gordonii and evaluation of native promoter strength using a multiple-copy plasmid." Canadian Journal of Microbiology 53, no. 3 (March 2007): 417–26. http://dx.doi.org/10.1139/w07-004.
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An active area of research in the development of Streptococcus gordonii for use as a bacterial commensal vector involves the identification and utilization of strong promoters for high-level expression of heterologous products. Escherichia coli plasmid vectors containing different streptococcal promoters often fail to become established in E. coli for unknown reasons. Therefore, it is desirable at times to transform S. gordonii, which is naturally competent, with small quantities of nascently ligated DNA without using E. coli first to amplify or screen the product. By comparing the efficiency of two methods used to induce competence in S. gordonii, it was shown that the use of a synthetic competence stimulating peptide substantially enhanced plasmid uptake by S. gordonii. We amplified the amylase-binding protein (abpA) promoter from the S. gordonii genome and, using a synthetic peptide to induce competence, directly introduced plasmid DNA containing this promoter into S. gordonii as an unamplified product of ligation. This plasmid facilitated abundant secretion of a heterologous product by S. gordonii. By assessing the levels of heterologous product secreted by two plasmid constructs, it was possible to evaluate the relative strength of two native promoters.
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Kuang, Xinyi, Tao Yang, Chenzi Zhang, Xian Peng, Yuan Ju, Chungen Li, Xuedong Zhou, Youfu Luo, and Xin Xu. "Repurposing Napabucasin as an Antimicrobial Agent against Oral Streptococcal Biofilms." BioMed Research International 2020 (November 20, 2020): 1–9. http://dx.doi.org/10.1155/2020/8379526.
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Objectives. Disruption of microbial biofilms is an effective way to control dental caries. Drug resistance and side effects of the existing antimicrobials necessitate the development of novel antibacterial agents. The current study was aimed at investigating the antibacterial activities of the repurposed natural compound napabucasin against oral streptococci. Methods. The minimum inhibitory concentration, minimum bactericidal concentration, minimum biofilm inhibition concentration, and minimum biofilm reduction concentration of Streptococcus mutans, Streptococcus gordonii, and Streptococcus sanguinis were examined by a microdilution method. Cytotoxicity of napabucasin against human oral keratinocytes, human gingival epithelia, and macrophage RAW264.7 was evaluated by CCK8 assays. The dead/live bacterium and exopolysaccharide in the napabucasin-treated multispecies biofilms were evaluated by confocal laser scanning microscopy. Microbial composition within the napabucasin-treated biofilms was further visualized by fluorescent in situ hybridization and qPCR. And the cariogenicity of napabucasin-treated biofilms was evaluated by transverse microradiography. Results. Napabucasin exhibited good antimicrobial activity against oral streptococcal planktonic cultures and biofilms but with lessened cytotoxicity as compared to chlorhexidine. Napabucasin reduced the cariogenic S. mutans and increased the proportion of the commensal S. gordonii in the multispecies biofilms. More importantly, napabucasin significantly reduced the demineralization capability of biofilms on tooth enamels. Conclusion. Napabucasin shows lessened cytotoxicity and comparable antimicrobial effects to chlorhexidine. Repurposing napabucasin may represent a promising adjuvant for the management of dental caries.
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Marquez, Ana Karen Lopez, Irene Meester, Johnny Rylander Yamada, Teresita de Jesus Mendez Quevedo, Rosa Isela Sanchez Najera, Rene Hernandez Delgadillo, Gustavo Israel Martinez González, Monica Sofia Treviño Ramirez, and Juan Manuel Solis Soto. "Streptococcus gordonii: An updated review." International Journal of Applied Dental Sciences 9, no. 1 (January 1, 2023): 80–83. http://dx.doi.org/10.22271/oral.2023.v9.i1b.1658.
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Lee, Song F., Yi-Jing Li, and Scott A. Halperin. "Overcoming codon-usage bias in heterologous protein expression in Streptococcus gordonii." Microbiology 155, no. 11 (November 1, 2009): 3581–88. http://dx.doi.org/10.1099/mic.0.030064-0.
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One of the limitations facing the development of Streptococcus gordonii into a successful vaccine vector is the inability of this bacterium to express high levels of heterologous proteins. In the present study, we have identified 12 codons deemed as rare codons in S. gordonii and seven other streptococcal species. tRNA genes encoding 10 of the 12 rare codons were cloned into a plasmid. The plasmid was transformed into strains of S. gordonii expressing the fusion protein SpaP/S1, the anti-complement receptor 1 (CR1) single-chain variable fragment (scFv) antibody, or the Toxoplasma gondii cyclophilin C18 protein. These three heterologous proteins contained high percentages of amino acids encoded by rare codons. The results showed that the production of SpaP/S1, anti-CR1 scFv and C18 increased by 2.7-, 120- and 10-fold, respectively, over the control strains. In contrast, the production of the streptococcal SpaP protein without the pertussis toxin S1 fragment was not affected by tRNA gene supplementation, indicating that the increased production of SpaP/S1 protein was due to the ability to overcome the limitation caused by rare codons required for the S1 fragment. The increase in anti-CR1 scFv production was also observed in Streptococcus mutans following tRNA gene supplementation. Collectively, the findings in the present study demonstrate for the first time, to the best of our knowledge, that codon-usage bias exists in Streptococcus spp. and the limitation of heterologous protein expression caused by codon-usage bias can be overcome by tRNA supplementation.
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Liu, Jinman, Chenggang Wu, I.-Hsiu Huang, Justin Merritt, and Fengxia Qi. "Differential response of Streptococcus mutans towards friend and foe in mixed-species cultures." Microbiology 157, no. 9 (September 1, 2011): 2433–44. http://dx.doi.org/10.1099/mic.0.048314-0.
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In the oral biofilm, the ‘mitis’ streptococci are among the first group of organisms to colonize the tooth surface. Their proliferation is thought to be an important factor required for antagonizing the growth of cariogenic species such as Streptococcus mutans. In this study, we used a three-species mixed culture to demonstrate that another ubiquitous early colonizing species, Veillonella parvula, can greatly affect the outcome of the competition between a pair of antagonists such as S. mutans and Streptococcus gordonii. Transcriptome analysis further revealed that S. mutans responds differentially to its friend (V. parvula) and foe (S. gordonii). In the mixed culture with S. gordonii, all but one of the S. mutans sugar uptake and metabolic genes were downregulated, while genes for alternative energy source utilization and H2O2 tolerance were upregulated, resulting in a slower but persistent growth. In contrast, when cultured with V. parvula, S. mutans grew equally well or better than in monoculture and exhibited relatively few changes within its transcriptome. When V. parvula was introduced into the mixed culture of S. mutans and S. gordonii, it rescued the growth inhibition of S. mutans. In this three-species environment, S. mutans increased the expression of genes required for the uptake and metabolism of minor sugars, while genes required for oxidative stress tolerance were downregulated. We conclude that the major factors that affect the competition between S. mutans and S. gordonii are carbohydrate utilization and H2O2 resistance. The presence of V. parvula in the tri-species culture mitigates these two major factors and allows S. mutans to proliferate, despite the presence of S. gordonii.
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Kreth, Jens, Hung Vu, Yongshu Zhang, and Mark C. Herzberg. "Characterization of Hydrogen Peroxide-Induced DNA Release by Streptococcus sanguinis and Streptococcus gordonii." Journal of Bacteriology 191, no. 20 (August 14, 2009): 6281–91. http://dx.doi.org/10.1128/jb.00906-09.
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ABSTRACT Extracellular DNA (eDNA) is produced by several bacterial species and appears to contribute to biofilm development and cell-cell adhesion. We present data showing that the oral commensals Streptococcus sanguinis and Streptococcus gordonii release DNA in a process induced by pyruvate oxidase-dependent production of hydrogen peroxide (H2O2). Surprisingly, S. sanguinis and S. gordonii cell integrity appears unaffected by conditions that cause autolysis in other eDNA-producing bacteria. Exogenous H2O2 causes release of DNA from S. sanguinis and S. gordonii but does not result in obvious lysis of cells. Under DNA-releasing conditions, cell walls appear functionally intact and ribosomes are retained over time. During DNA release, intracellular RNA and ATP are not coreleased. Hence, the release mechanism appears to be highly specific for DNA. Release of DNA without detectable autolysis is suggested to be an adaptation to the competitive oral biofilm environment, where autolysis could create open spaces for competitors to invade. Since eDNA promotes cell-to-cell adhesion, release appears to support oral biofilm formation and facilitates exchange of genetic material among competent strains.
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Vriesema, Aldwin J. M., Jacob Dankert, and Sebastian A. J. Zaat. "A Shift from Oral to Blood pH Is a Stimulus for Adaptive Gene Expression of Streptococcus gordonii CH1 and Induces Protection against Oxidative Stress and Enhanced Bacterial Growth by Expression of msrA." Infection and Immunity 68, no. 3 (March 1, 2000): 1061–68. http://dx.doi.org/10.1128/iai.68.3.1061-1068.2000.
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ABSTRACT Viridans group streptococci (VS) from the oral cavity entering the bloodstream may initiate infective endocarditis (IE). We aimed to identify genes expressed in response to a pH increase from slightly acidic (pH 6.2) to neutral (pH 7.3) as encountered by VS entering the bloodstream from the oral cavity. Using a recently developed promoter-screening vector, we isolated five promoter fragments from the genomic DNA of Streptococcus gordonii CH1 responding to this stimulus. No common regulatory sequences were identified in these promoter fragments that could account for the coordinate expression of the corresponding genes. One of the isolated fragments contained the promoter region and 5′ end of a gene highly homologous to the methionine sulfoxide reductase gene (msrA) of various bacterial and eukaryotic species. This gene has been found to be activated in S. gordonii strain V288 in a rabbit model of IE (A. O. Kiliç, M. C. Herzberg, M. W. Meyer, X. Zhao, and L. Tao, Plasmid 42:67–72, 1999). We isolated and characterized the msrA gene of S. gordonii CH1 and constructed a chromosomal insertion mutant. This mutant was more sensitive to hydrogen peroxide, suggesting a role for the streptococcal MsrA in protecting against oxidative stress. Moreover, MsrA appeared to be important for the growth of S. gordonii CH1 under aerobic and anaerobic conditions. Both these properties of MsrA may contribute to the ability of S. gordonii to cause IE.
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Ahn, S. J., H. S. Kho, S. W. Lee, and D. S. Nahm. "Roles of Salivary Proteins in the Adherence of Oral Streptococci to Various Orthodontic Brackets." Journal of Dental Research 81, no. 6 (June 2002): 411–15. http://dx.doi.org/10.1177/154405910208100611.
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Knowledge of salivary pellicles on orthodontic brackets provides a better understanding of microbial adherence. The aim of this study was to analyze the effects of bracket pellicles on the adherence of Streptococcus gordonii and Streptococcus mutans. Bracket pellicles were formed by the incubation of 4 kinds of orthodontic brackets with unstimulated whole saliva for 2 hrs, and analyzed by electrophoresis, immunodetection, and amino acid analysis. Binding assays were then performed by the incubation of tritium-labeled streptococci with the pellicle-transfer blots and orthodontic brackets. The results showed that low-molecular-weight mucin, α-amylase, secretory IgA, acidic proline-rich proteins, and cystatins adhered to all kinds of brackets, though the amino acid composition of pellicles differed between bracket types. Some of these proteins increased the binding of S. gordonii to saliva-coated brackets. However, salivary pellicles decreased the binding of S. mutans. Collectively, salivary pellicles were found to play a significant role in the initial adhesion of oral streptococci to orthodontic brackets.
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Vickerman, M. M., S. E. Flannagan, A. M. Jesionowski, K. A. Brossard, D. B. Clewell, and C. M. Sedgley. "A Genetic Determinant in Streptococcus gordonii Challis Encodes a Peptide with Activity Similar to That of Enterococcal Sex Pheromone cAM373, Which Facilitates Intergeneric DNA Transfer." Journal of Bacteriology 192, no. 10 (March 16, 2010): 2535–45. http://dx.doi.org/10.1128/jb.01689-09.
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ABSTRACT Enterococcus faecalis strains secrete multiple peptides representing different sex pheromones that induce mating responses by bacteria carrying specific conjugative plasmids. The pheromone cAM373, which induces a response by the enterococcal plasmid pAM373, has been of interest because a similar activity is also secreted by Streptococcus gordonii and Staphylococcus aureus. The potential to facilitate intergeneric DNA transfer from E. faecalis is of concern because of extensive multiple antibiotic resistance, including vancomycin resistance, that has emerged among enterococci in recent years. Here, we characterize the related pheromone determinant in S. gordonii and show that the peptide it encodes, gordonii-cAM373, does indeed induce transfer of plasmid DNA from E. faecalis into S. gordonii. The streptococcal determinant camG encodes a lipoprotein with a leader sequence, the last 7 residues of which represent the gordonii-cAM373 heptapeptide SVFILAA. Synthetic forms of the peptide had activity similar to that of the enterococcal cAM373 AIFILAS. The lipoprotein moiety bore no resemblance to the lipoprotein encoded by E. faecalis. We also identified determinants in S. gordonii encoding a signal peptidase and an Eep-like zinc metalloprotease (lspA and eep, respectively) similar to those involved in processing certain pheromone precursors in E. faecalis. Mutations generated in camG, lspA, and eep each resulted in the ablation of gordonii-cAM373 activity in culture supernatants. This is the first genetic analysis of a potential sex pheromone system in a commensal oral streptococcal species, which may have implications for intergeneric gene acquisition in oral biofilms.
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Young Lee, Si, John O. Cisar, Joseph L. Bryant, Michael A. Eckhaus, and Ann L. Sandberg. "Resistance of Streptococcus gordonii to Polymorphonuclear Leukocyte Killing Is a Potential Virulence Determinant of Infective Endocarditis." Infection and Immunity 74, no. 6 (June 2006): 3148–55. http://dx.doi.org/10.1128/iai.00087-06.
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ABSTRACT Significant differences in virulence among seven representative Streptococcus gordonii strains were observed by using the rat model of infective endocarditis. Five strains, including S. gordonii DL1, caused severe disease, while the other two strains, including S. gordonii SK12, caused minimal or no disease. The differences in virulence were evident from the visible presence of streptococci in the vegetations present on the aortic valves of catheterized rats that were challenged with individual strains and also from the much greater recovery of rifampin-resistant S. gordonii DLl than of streptomycin-resistant S. gordonii SK12 from the hearts of animals coinfected with both organisms. Each S. gordonii strain aggregated with human platelets and bound to polymorphonuclear leukocytes (PMNs), as shown by the stimulation of PMN superoxide anion production. These interactions were reduced or abolished by pretreatment of the platelets or PMNs with sialidase, indicating that there was bacterial recognition of host sialic acid-containing receptors. Adhesin-mediated binding of each S. gordonii strain to PMNs also triggered phagocytosis. However, the subsequent PMN-dependent killing differed significantly for the seven strains. The five virulent strains included three strains that were not killed and two strains whose numbers were reduced by approximately 50%. In contrast, the level of killing of each avirulent strain under the same conditions was significantly greater and approached 90% of the bacteria added. Parallel studies performed with rat PMNs revealed comparable differences in the resistance or susceptibility of representative virulent and avirulent strains. Thus, the ability of S. gordonii to survive in PMNs following adhesin-mediated phagocytosis may be an important virulence determinant of infective endocarditis.
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Park, Ok-Jin, Yeongkag Kwon, Chaeyeon Park, Yoon Ju So, Tae Hwan Park, Sungho Jeong, Jintaek Im, Cheol-Heui Yun, and Seung Hyun Han. "Streptococcus gordonii: Pathogenesis and Host Response to Its Cell Wall Components." Microorganisms 8, no. 12 (November 24, 2020): 1852. http://dx.doi.org/10.3390/microorganisms8121852.
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Streptococcus gordonii, a Gram-positive bacterium, is a commensal bacterium that is commonly found in the skin, oral cavity, and intestine. It is also known as an opportunistic pathogen that can cause local or systemic diseases, such as apical periodontitis and infective endocarditis. S. gordonii, an early colonizer, easily attaches to host tissues, including tooth surfaces and heart valves, forming biofilms. S. gordonii penetrates into root canals and blood streams, subsequently interacting with various host immune and non-immune cells. The cell wall components of S. gordonii, which include lipoteichoic acids, lipoproteins, serine-rich repeat adhesins, peptidoglycans, and cell wall proteins, are recognizable by individual host receptors. They are involved in virulence and immunoregulatory processes causing host inflammatory responses. Therefore, S.gordonii cell wall components act as virulence factors that often progressively develop diseases through overwhelming host responses. This review provides an overview of S. gordonii, and how its cell wall components could contribute to the pathogenesis and development of therapeutic strategies.
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Zhang, Yongshu, Marvin Whiteley, Jens Kreth, Yu Lei, Ali Khammanivong, Jamie N. Evavold, Jingyuan Fan, and Mark C. Herzberg. "The two-component system BfrAB regulates expression of ABC transporters in Streptococcus gordonii and Streptococcus sanguinis." Microbiology 155, no. 1 (January 1, 2009): 165–73. http://dx.doi.org/10.1099/mic.0.023168-0.
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The putative two-component system BfrAB is involved in Streptococcus gordonii biofilm development. Here, we provide evidence that BfrAB regulates the expression of bfrCD and bfrEFG, which encode two ATP-binding cassette (ABC) transporters, and bfrH, which encodes a CAAX amino-terminal protease family protein. BfrC and BfrE are ATP-binding proteins, and BfrD, BfrF and BfrG are homologous membrane-spanning polypeptides. Similarly, BfrABss, the BfrAB homologous system in Streptococcus sanguinis, controls the expression of two bfrCD-homologous operons (bfrCD ss and bfrXY ss), a bfrH-homologous gene (bfrH1 ss) and another CAAX amino-terminal protease family protein gene (bfrH2ss ). Furthermore, we demonstrate that the purified BfrA DNA-binding domain from S. gordonii binds to the promoter regions of bfrCD, bfrEFG, bfrH, bfrCD ss, bfrXY ss and bfrH1 ss in vitro. Finally, we show that the BfrA DNA-binding domain recognizes a conserved DNA motif with a consensus sequence of TTTCTTTAGAAATATTTTAGAATT. These data suggest, therefore, that S. gordonii BfrAB controls biofilm formation by regulating multiple ABC-transporter systems.
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Baca, Katia, Hebert Puente, Franco González, Katherine Leyva, Bruno Rodriguez, and Félix Medina. "Endocarditis infecciosa secundaria a Streptococcus gordonii, complicada con aneurisma y fístula en válvula mitral. Reporte de caso." Revista Medica Herediana 28, no. 1 (April 17, 2017): 37. http://dx.doi.org/10.20453/rmh.v28i1.3072.
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Entre las bacterias poco comunes que causan Endocarditis infecciosa (EI), se encuentran el Streptococcus gordonii, conocido por su habilidad de colonizar y dañar las válvulas cardiacas. Asimismo, se conoce que el hallazgo de aneurisma complicado con fístula intracardiaca es infrecuente en EI, sólo se presenta en el 1,6% de pacientes. Se reporta el caso de un varón de 58 años con EI por Streptococcus gordonii complicada con aneurisma y fístula en la válvula mitral.
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Pellerin, Geneviève, Laurent Bazinet, and Daniel Grenier. "Deacidification of Cranberry Juice Reduces Its Antibacterial Properties against Oral Streptococci but Preserves Barrier Function and Attenuates the Inflammatory Response of Oral Epithelial Cells." Foods 10, no. 7 (July 15, 2021): 1634. http://dx.doi.org/10.3390/foods10071634.
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Cranberry (Vaccinium macrocarpon) may be a potent natural adjuvant for the prevention of oral diseases due to its anti-adherence, anti-cariogenic, and anti-inflammatory properties. However, the high titrable acidity of cranberry juice (CJ) has been reported to cause gastrointestinal discomfort, leading consumers to restrict their intake of this beverage. Electrodialysis with a bipolar membrane (EDBM) can reduce the organic acid content of CJ while retaining the flavonoids associated with potential health benefits. This study aimed to assess how the deacidification of CJ by EDBM impacts the antibacterial properties of the beverage against cariogenic (Streptococcus mutans, Streptococcus sobrinus) and commensal (Streptococcus gordonii, Streptococcus oralis, Streptococcus salivarius) streptococci, and how it affects oral epithelial barrier function and inflammatory response in an in vitro model. The removal of organic acids from CJ (deacidification rate ≥42%) reduced the bactericidal activity of the beverage against planktonic S. mutans and S. gordonii after a 15-min exposure, whereas only the viability of S. gordonii was significantly impacted by CJ deacidification rate when the bacteria were embedded in a biofilm. Moreover, conditioning saliva-coated hydroxyapatite with undiluted CJ samples significantly lowered the adherence of S. mutans, S. sobrinus, and S. oralis. With respect to epithelial barrier function, exposure to CJ deacidified at a rate of ≥19% maintained the integrity of a keratinocyte monolayer over the course of 24 h compared to raw CJ, as assessed by the determination of transepithelial electrical resistance (TER) and fluorescein isothiocyanate-conjugated dextran paracellular transport. These results can be in part attributed to the inability of the deacidified CJ to disrupt two tight junction proteins, zonula occludens−1 and occludin, following exposure, unlike raw CJ. Deacidification of CJ impacted the secretion of IL-6, but not of IL-8, by oral epithelial cells. In conclusion, deacidification of CJ appears to provide benefits with respect to the maintenance of oral health.
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Fujiwara, Taku, Tomonori Hoshino, Takashi Ooshima, Shizuo Sobue, and Shigeyuki Hamada. "Purification, Characterization, and Molecular Analysis of the Gene Encoding Glucosyltransferase fromStreptococcus oralis." Infection and Immunity 68, no. 5 (May 1, 2000): 2475–83. http://dx.doi.org/10.1128/iai.68.5.2475-2483.2000.
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ABSTRACT Streptococcus oralis is a member of the oral streptococcal family and an early-colonizing microorganism in the oral cavity of humans. S. oralis is known to produce glucosyltransferase (GTase), which synthesizes glucans from sucrose. The enzyme was purified chromatographically from a culture supernatant of S. oralis ATCC 10557. The purified enzyme, GTase-R, had a molecular mass of 173 kDa and a pI of 6.3. This enzyme mainly synthesized water-soluble glucans with no primer dependency. The addition of GTase markedly enhanced the sucrose-dependent resting cell adhesion of Streptococcus mutans at a level similar to that found in growing cells of S. mutans. The antibody against GTase-R inhibited the glucan-synthesizing activities ofStreptococcus gordonii and Streptococcus sanguis, as well as S. oralis. The N-terminal amino acid sequence of GTase-R exhibited no similarities to known GTase sequences of oral streptococci. Using degenerate PCR primers, an 8.1-kb DNA fragment, carrying the gene (gtfR) coding for GTase-R and its regulator gene (rgg), was cloned and sequenced. Comparison of the deduced amino acid sequence revealed that thergg genes of S. oralis and S. gordonii exhibited a close similarity. The gtfR gene was found to possess a species-specific nucleotide sequence corresponding to the N-terminal 130 amino acid residues. Insertion oferm or aphA into the rgg orgtfR gene resulted in decreased GTase activity by the organism and changed the colony morphology of these transformants. These results indicate that S. oralis GTase may play an important role in the subsequent colonizing of mutans streptoccoci.
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Loo, C. Y., D. A. Corliss, and N. Ganeshkumar. "Streptococcus gordonii Biofilm Formation: Identification of Genes that Code for Biofilm Phenotypes." Journal of Bacteriology 182, no. 5 (March 1, 2000): 1374–82. http://dx.doi.org/10.1128/jb.182.5.1374-1382.2000.
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ABSTRACT Viridans streptococci, which include Streptococcus gordonii, are pioneer oral bacteria that initiate dental plaque formation. Sessile bacteria in a biofilm exhibit a mode of growth that is distinct from that of planktonic bacteria. Biofilm formation ofS. gordonii Challis was characterized using an in vitro biofilm formation assay on polystyrene surfaces. The same assay was used as a nonbiased method to screen isogenic mutants generated by Tn916 transposon mutagenesis for defective biofilm formation. Biofilms formed optimally when bacteria were grown in a minimal medium under anaerobic conditions. Biofilm formation was affected by changes in pH, osmolarity, and carbohydrate content of the growth media. Eighteen biofilm-defective mutants ofS. gordonii Challis were identified based on Southern hybridization with a Tn916-based probe and DNA sequences of the Tn916-flanking regions. Molecular analyses of these mutants showed that some of the genes required for biofilm formation are involved in signal transduction, peptidoglycan biosynthesis, and adhesion. These characteristics are associated with quorum sensing, osmoadaptation, and adhesion functions in oral streptococci. Only nine of the biofilm-defective mutants had defects in genes of known function, suggesting that novel aspects of bacterial physiology may play a part in biofilm formation. Further identification and characterization of biofilm-associated genes will provide insight into the molecular mechanisms of biofilm formation of oral streptococci.
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AM, Khairuldin, Ibrahim IK, Wakiyuddin SB, Wenning Z, Lesley AO, Nicholas SJ, and Siew WC. "Genome Analysis of Streptococcus gordonii SK12." Annals of Dentistry 21, no. 2 (December 31, 2014): 17–26. http://dx.doi.org/10.22452/adum.vol21no2.1.
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Tanzer, J. M., A. Thompson, K. Sharma, M. M. Vickerman, E. M. Haase, and F. A. Scannapieco. "Streptococcus mutansOut-competesStreptococcus gordonii in vivo." Journal of Dental Research 91, no. 5 (March 19, 2012): 513–19. http://dx.doi.org/10.1177/0022034512442894.
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Nairn, Brittany L., Grace T. Lee, Ashwani K. Chumber, Patrick R. Steck, Mahmoud O. Mire, Bruno P. Lima, and Mark C. Herzberg. "Uncovering Roles of Streptococcus gordonii SrtA-Processed Proteins in the Biofilm Lifestyle." Journal of Bacteriology 203, no. 2 (October 26, 2020): e00544-20. http://dx.doi.org/10.1128/jb.00544-20.
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ABSTRACTStreptococcus gordonii is a commensal oral organism. Harmless in the oral cavity, S. gordonii is an opportunistic pathogen. S. gordonii adheres to body surfaces using surface adhesive proteins (adhesins), which are critical to subsequent formation of biofilm communities. As in most Gram-positive bacteria, S. gordonii surface proteins containing the C-terminal LPXTG motif cleavage sequence are processed by sortase A (SrtA) to become covalently attached to the cell wall. To characterize the functional diversity and redundancy in the family of SrtA-processed proteins, an S. gordonii DL1 markerless deletion mutant library was constructed of each of the 26 putative SrtA-processed proteins. Each library member was evaluated for growth in rich medium, biofilm formation on plastic, saliva and salivary fractions, cell surface hydrophobicity (CSH), hemagglutination, and integration into an ex vivo plaque biofilm community. Library members were compared to the non-SrtA-processed adhesins AbpA and AbpB. While no major growth differences in rich medium were observed, many S. gordonii LPXTG/A proteins impacted biofilm formation on one or more of the substrates. Several mutants showed significant differences in hemagglutination, hydrophobicity, or fitness in the ex vivo plaque model. From the identification of redundant and unique functions in these in vitro and ex vivo systems, functional stratification among the LPXTG/A proteins is apparent.IMPORTANCES. gordonii interactions with its environment depend on the complement of cell wall proteins. A subset of these cell wall proteins requires processing by the enzyme sortase A (SrtA). The identification of SrtA-processed proteins and their functional characterization will help the community to better understand how S. gordonii engages with its surroundings, including other microbes, integrates into the plaque community, adheres to the tooth surface, and hematogenously disseminates to cause blood-borne infections. This study identified 26 putative SrtA-processed proteins through creation of a markerless deletion mutant library. The library was subject to functional screens that were chosen to better understand key aspects of S. gordonii physiology and pathogenesis.
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Flowers, Robert Costigan, Beatriz Rivera Rodriguez, and Kelly Corbitt. "Streptococcus gordonii septic arthritis of the glenohumeral joint following deltoid intramuscular vaccination." BMJ Case Reports 14, no. 5 (May 2021): e243066. http://dx.doi.org/10.1136/bcr-2021-243066.
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A 68-year-old woman presented for left shoulder pain, decreased range of motion (ROM) and fever 7 days following COVID-19 vaccination. Investigations showed a tender left deltoid mass, decreased shoulder ROM and elevated inflammatory markers. MRI demonstrated a large glenohumeral effusion with synovitis, and arthrocentesis confirmed septic arthritis (SA). She required subtotal bursectomy. Intraoperative joint cultures grew Streptococcus gordonii. She completed 6 weeks of antibiotics and is undergoing physical therapy for post-infectious adhesive capsulitis. SA is most commonly due to Staphylococcus aureus and β-haemolytic streptococci, and rarely due to viridans group streptococci including S. gordonii. To avoid inadvertent injection into the glenohumeral joint, vaccination should be performed posteriorly and inferiorly into the deltoid musculature. Progressive pain, fever or decreased passive ROM following vaccination should raise concern for SA. Given its rarity, however, concern for secondary SA should not affect the general population’s consideration for vaccination.