Academic literature on the topic 'Streptococcus gordonii'

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Journal articles on the topic "Streptococcus gordonii"

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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'.
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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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Dissertations / Theses on the topic "Streptococcus gordonii"

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Christie, Julie. "Fibronectin-interacting proteins in Streptococcus gordonii." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324360.

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Macarthur, Deborah Jane. "Mapping The Proteome Of Streptococcus Gordonii." Thesis, The University of Sydney, 2005. http://hdl.handle.net/2123/5097.

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Streptococcus gordonii is a primary coloniser of the tooth surface where it efficiently ferments carbohydrates at pH levels above 6.0. By not being able to maintain the pH of dental plaque to a level required for enamel dissolution, the dominance of S. gordonii in dental plaque is considered a sign of a healthy oral cavity. However, upon entering the bloodstream and encountering a rise in pH, S. gordonii may become pathogenic, being one of the major causative organisms associated with infective endocarditis. Proteome analyses of S. gordonii grown at steady state in a chemostat allowed the phenotypic changes associated with alterations in pH levels characteristic of these two environments to be determined. As an initial starting point to this study, a two-dimensional electrophoresis (2- DE) reference map of S. gordonii grown at pH 7.0 was produced. Although only 50% of the S gordonii genome was available in an annotated form during the course of this study, the closely related Streptococcus pneumoniae genome (with which S. gordonii shares 97.24% DNA sequence homology) had been completed in 2001. The use of both of these databases allowed many of the S. gordonii proteins to be identified by mass spectrometry. Four hundred and seventy six protein spots, corresponding to 250 different proteins, or 12.5% of the S. gordonii proteome, were identified, giving rise to the first comprehensive proteome reference map of this oral bacterium. Of the 250 different proteins, 196 were of cellular origin while 68 were identified from the extracellular milieu. Only 14 proteins were common to both compartments. Of particular interest among the 54 uniquely identified extracellular proteins was a homologue of a peptidoglycan hydrolase that has been associated with virulence in S. pneumoniae. Among the other proteins identified were ones involved in transport and binding, energy metabolism, translation, transformation, stress response and virulence. Twelve cell envelope proteins were identified as well as 25 others that were predicted to have a membrane association based on the presence of at least one transmembrane domain. The study also confirmed the existence of 38 proteins previously designated as �hypothetical� or with no known function. Mass spectral data for over 1000 protein spots were accumulated and archived for future analysis when sequencing of the S. gordonii genome is finally completed. Following the mapping of the proteome of S. gordonii, alterations in protein spots associated with growth of the bacterium at pH intervals of 0.5 units in the pH range 5.5 - 7.5 were determined. Only 16 protein spots were shown to be significantly altered in their level of expression despite the range of pH studied. Among the differentially expressed proteins was a manganese-dependent inorganic pyrophosphatase (PpaC), which regulates expression of adhesins required for coaggregation. The expression of PpaC was highest at pH 6.5 - 7.0, the pH of a healthy oral cavity, indicating that PpaC may play an important part in dental plaque formation. Another differentially expressed protein was the heat-inducible transcription repressor (HrcA). Alterations in HrcA were consistent with its role as a negative repressor in regulating heat-shock proteins at low pH, even though no changes in the level of heat-shock proteins were observed as the pH declined. This result gave rise to the hypothesis that the possible reason cariogenic bacteria, such as Streptococcus mutans, can out compete S. gordonii at low pH might simply be due to their ability to manipulate their proteome in a complex manner for survival and persistence at low pH, unlike S. gordonii. This may imply some prevailing level of genetic regulation that is missing in S. gordonii.
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Macarthur, Deborah Jane. "Mapping the proteome of Streptococcus gordonii." University of Sydney. Health Science, 2005. http://hdl.handle.net/2123/686.

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Streptococcus gordonii is a primary coloniser of the tooth surface where it efficiently ferments carbohydrates at pH levels above 6.0. By not being able to maintain the pH of dental plaque to a level required for enamel dissolution, the dominance of S. gordonii in dental plaque is considered a sign of a healthy oral cavity. However, upon entering the bloodstream and encountering a rise in pH, S. gordonii may become pathogenic, being one of the major causative organisms associated with infective endocarditis. Proteome analyses of S. gordonii grown at steady state in a chemostat allowed the phenotypic changes associated with alterations in pH levels characteristic of these two environments to be determined. As an initial starting point to this study, a two-dimensional electrophoresis (2- DE) reference map of S. gordonii grown at pH 7.0 was produced. Although only 50% of the S gordonii genome was available in an annotated form during the course of this study, the closely related Streptococcus pneumoniae genome (with which S. gordonii shares 97.24% DNA sequence homology) had been completed in 2001. The use of both of these databases allowed many of the S. gordonii proteins to be identified by mass spectrometry. Four hundred and seventy six protein spots, corresponding to 250 different proteins, or 12.5% of the S. gordonii proteome, were identified, giving rise to the first comprehensive proteome reference map of this oral bacterium. Of the 250 different proteins, 196 were of cellular origin while 68 were identified from the extracellular milieu. Only 14 proteins were common to both compartments. Of particular interest among the 54 uniquely identified extracellular proteins was a homologue of a peptidoglycan hydrolase that has been associated with virulence in S. pneumoniae. Among the other proteins identified were ones involved in transport and binding, energy metabolism, translation, transformation, stress response and virulence. Twelve cell envelope proteins were identified as well as 25 others that were predicted to have a membrane association based on the presence of at least one transmembrane domain. The study also confirmed the existence of 38 proteins previously designated as �hypothetical� or with no known function. Mass spectral data for over 1000 protein spots were accumulated and archived for future analysis when sequencing of the S. gordonii genome is finally completed. Following the mapping of the proteome of S. gordonii, alterations in protein spots associated with growth of the bacterium at pH intervals of 0.5 units in the pH range 5.5 - 7.5 were determined. Only 16 protein spots were shown to be significantly altered in their level of expression despite the range of pH studied. Among the differentially expressed proteins was a manganese-dependent inorganic pyrophosphatase (PpaC), which regulates expression of adhesins required for coaggregation. The expression of PpaC was highest at pH 6.5 - 7.0, the pH of a healthy oral cavity, indicating that PpaC may play an important part in dental plaque formation. Another differentially expressed protein was the heat-inducible transcription repressor (HrcA). Alterations in HrcA were consistent with its role as a negative repressor in regulating heat-shock proteins at low pH, even though no changes in the level of heat-shock proteins were observed as the pH declined. This result gave rise to the hypothesis that the possible reason cariogenic bacteria, such as Streptococcus mutans, can out compete S. gordonii at low pH might simply be due to their ability to manipulate their proteome in a complex manner for survival and persistence at low pH, unlike S. gordonii. This may imply some prevailing level of genetic regulation that is missing in S. gordonii.
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Jack, Alison Alexandra. "Signalling interactions between Streptococcus gordonii and Candida albicans." Thesis, University of Bristol, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.633446.

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Streptococcus gordonii is an early bacterial coloniser of the oral cavity and influences development of plaque biofilms. Interactions of Candida albicans, an opportunistic fungal pathogen, with S. gordonii are hypothesised to promote fungal carriage and persistence. Evidence suggests that signalling molecules produced by streptococci, including competence stimulating peptide (eSP) and autoinducer 2 (AI -2L affect C. albicans growth. However, less is understood about the molecular basis of these interactions.
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Forsgren, Nina. "Structural studies of the surface adhesin SspB from Streptococcus gordonii." Doctoral thesis, Umeå : Umeå universitet, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-32910.

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Ilias, Mohammad. "Family II soluble inorganic pyrophosphatases from 'Streptococcus gordonii' and 'Vibrio cholerae'." Thesis, University of Birmingham, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.410862.

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Robinson, Jill Christie. "Impact of L-arginine on Streptococcus gordonii gene expression and biofilm formation." Thesis, University of Newcastle upon Tyne, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.701159.

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Streptococcus gordonii is an oral commensal bacterium, and an early coloniser of the acquired salivary pellicle that coats tooth surfaces. As such, it is a key organism in the establishment of dental plaque biofilms. The amino acid L-arginine has been previously shown to play a role in biofilm formation in other oral species, and depletion of L-arginine has a significant impact upon S. gordonii growth and gene regulation. Three L-arginine-dependent transcription regulators have been identified in S. gordonii, but it is currently not clear how these co-ordinate to sense and respond to changes in the exogenous L-arginine concentration. Therefore, the major aims of this work were to (i) further elucidate the impacts of L-arginine on S. gordonii growth and biofilm formation, (ii) investigate the roles of three putative arginine-dependent regulators in modulating arginine-responsive gene regulation, and (iii) assess the effects of L-arginine-dependent gene regulators on S. gordonii biofilm formation. Initial growth experiments revealed that high concentrations (≥500 mM) of L-arginine retard S. gordonii planktonic growth in a chemically defined medium, resulting in lower growth yields than intermediate (0.5 mM) L-arginine. However, 500 mM L-arginine was not toxic to S. gordonii cells incubated in natural human saliva. S. gordonii has previously been shown to be conditionally auxotrophic for L-arginine, since it can biosynthesise L-arginine under strictly anaerobic conditions or during the gradual depletion of extracellular L-arginine, but it cannot grow following a rapid shift to medium lacking L-arginine. A similar lack of growth was also found following rapid depletion of L-histidine and the branched-chain amino acids. S. gordonii is predicted to encode all genes required for L-histidine and branched chain amino acids, and it is possible that this organism is conditionally auxotrophic for multiple amino acids. Rapid depletion of L-arginine was shown previously to result in a change in expression of >20% of the S. gordonii genome. By comparing expression levels of some of the most strongly arginine-regulated genes when cells were challenged with depletion of L-histidine or branched chain amino acids, it was shown that some of the genes (for example, argC, SGO_1686, asp5) were specifically regulated by arginine depletion, whereas others (bfbF, SGO_1699) were similarly regulated following depletion of all amino acids. Therefore, it appears that depletion of L-arginine results in both an arginine-specific response and a more generalised stress response, presumably associated with growth arrest in this medium. iv Investigation of the roles of three arginine-dependent regulators (ArcR, ArgR and AhrC) by gene expression microarrays identified a number of genes that were arginine-responsive and were differentially-regulated in the wild-type compared with the isogenic mutants ΔarcR, ΔargR or ΔahrC. There was extensive overlap between the genes regulated by the ArgR and AhrC regulators, suggesting that these regulators perform similar and interdependent roles in S. gordonii. Regulatory responses following arcR disruption were distinct from those seen in the argR and ahrC mutants. In addition to three loci that have previously been described, one particular gene, SGO_0846, encoding a hypothetical protein, was highly up-regulated in response to arcR deletion. This thesis is the first holistic study of the three arginine-dependent regulators in S. gordonii, and shows that each one plays a key role in arginine-dependent gene regulation. Finally, previous unpublished work from our group had demonstrated that S. gordonii ΔarcR displayed a defective biofilm phenotype, whereas the deletion strains of the other two regulators showed no such phenotype. To determine whether up-regulation of SGO_0846 is responsible for the biofilm attenuation in S. gordonii ΔarcR, a deletion mutant of SGO_0846 was constructed in both the wild-type and ΔarcR background. Disruption of the SGO_0846 gene showed no significant differences in biofilm formation levels in comparison to the wild-type background, and showed no effect on the biofilm defective phenotype of the ΔarcR mutant. This suggests that changes in expression of SGO_0846 are not responsible for the biofilm defects seen in the ΔarcR knockout, and that the ArcR regulator is affecting biofilm formation via another mechanism. In conclusion, this thesis provides evidence that arginine has a clear impact on gene expression and biofilm formation in S. gordonii, and furthermore, that the ArcR regulator is critical for optimal biofilm formation. It is possible that in the future, this could be used as a target for controlling S. gordonii biofilm formation, and subsequent dental plaque development.
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O'Connell, Silverman Richard James. "Molecular basis of mixed-species biofilm formation between streptococcus gordonii and candida albicans." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.529889.

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Higashi, Daniela. "Modulação do biofilme de Porphyromonas gingivalis pela associação com Streptococcus gordonii e com Prevotella intermedia." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/42/42132/tde-10042015-123236/.

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P. gingivalis é um dos principais patógenos da doença periodontal, é encontrado em biofilmes orais com S. gordonii e P. intermedia e em células endoteliais da artéria coronária in vivo. P. gingivalis necessita de ferro em seu metabolismo e pode usar certas proteínas do hospedeiro como fontes deste íon em ambientes limitantes. Assim, este estudo investigou o papel dos genes PGN0741/PG0637 (receptor dependente de TonB) e PGN0531/PG1380 (fvW) de P. gingivalis na formação de biofilme em diferentes concentrações de ferro, em biofilmes mistos com S. gordonii e P. intermedia, e na adesão e invasão de células endoteliais da artéria coronária. Os resultados mostraram divergências no papel dos genes TonB e fvW na formação dos monobiofilmes e mistos e em diferentes concentrações de ferro, demonstrando uma relação cepa-dependente. Na adesão, fvW se mostrou importante para ambas cepas, mas na persistência apenas para P. gingivalis W83. Este trabalho enfatiza, assim, a necessidade do uso de mais de uma cepa de P. gingivalis no estudo do papel de genes em ensaios experimentais.
P. gingivalis is one of the major pathogens of periodontal diseases. It is found in oral biofilms associated with S. gordonii and P. intermedia, and inside of coronary artery endothelial cells in vivo. P. gingivalis requires iron for growth and can exploit iron-carrying proteins of the host as sources in limiting environments. Thus, this work aimed to study the role of genes PGN0741/PG0637 (TonB-dependent receptor) and PGN0531/PG1380 (fvW) of P. gingivalis in biofilm formation under different iron concentrations, in mixed biofilms with S. gordonii and P. intermedia, and in the adhesion and invasion of coronary artery endothelial cells. Our data showed discordance for the role of TonB and fvW in homo- and heterotypic biofilm formation and in different iron concentrations. The relevance of both genes was strain-dependent. Gene fvW was relevant for adhesion to endothelial cells, but only for strain W83 during persistence. Therefore, our study emphasizes the importance of using different strains for a better understanding of the role of genes in experimental assays.
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Nylander, Åsa, Gunnel Svensäter, Dilani B. Senadheera, Dennis G. Cvitkovitch, Julia R. Davies, and Karina Persson. "Structural and functional analysis of the N-terminal domain of the Streptococcus gordonii adhesin Sgo0707." Umeå universitet, Oral mikrobiologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-71563.

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The commensal Streptococcus gordonii expresses numerous surface adhesins with which it interacts with other microorganisms, host cells and salivary proteins to initiate dental plaque formation. However, this Gram-positive bacterium can also spread to non-oral sites such as the heart valves and cause infective endocarditis. One of its surface adhesins, Sgo0707, is a large protein composed of a non-repetitive N-terminal region followed by several C-terminal repeat domains and a cell wall sorting motif. Here we present the crystal structure of the Sgo0707 N-terminal domains, refined to 2.1 Å resolution. The model consists of two domains, N1 and N2. The largest domain, N1, comprises a putative binding cleft with a single cysteine located in its centre and exhibits an unexpected structural similarity to the variable domains of the streptococcal Antigen I/II adhesins. The N2-domain has an IgG-like fold commonly found among Gram-positive surface adhesins. Binding studies performed on S. gordonii wild-type and a Sgo0707 deficient mutant show that the Sgo0707 adhesin is involved in binding to type-1 collagen and to oral keratinocytes.
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Books on the topic "Streptococcus gordonii"

1

Obinwa, Ngozika Kanayo. Identification and cloning of Streptococcus gordonii LGR2 and Streptococcus crista CR311 genes encoding their coaggregations with other oral bacteria. Manchester: University of Manchester, 1996.

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Whittaker, Catherine Jill. Identification and cloning of Streptococcus gordonii LGR2 genes encoding adhesins for saliva-coated hydroxyapatite (SHA). Manchester: University of Manchester, 1993.

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Shirkhodaee, Mohammad Masoud. Isolation of a DNA probe for the identification of the tooth surface adhesin gene(s) of Streptococcus gordonii LGR2. Manchester: University of Manchester, 1994.

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Vidyasanker, Radhika. The rpsL gene and streptomycin resistance in Streptococcus gordonii and Streptococcus pyogenes. 1999.

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Book chapters on the topic "Streptococcus gordonii"

1

Vickerman, M. M., and D. B. Clewell. "Regulation of Streptococcus gordonii Glucosyltransferase." In Streptococci and the Host, 661–64. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1825-3_154.

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Shiroza, Teruaki, and Howard Kuramitsu. "Secretion of heterologous proteins by genetically engineered Streptococcus gordonii." In Methods for studying the genetics, molecular biology, physiology, and pathogenesis of the streptococci, 127–36. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-017-2258-2_15.

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Pozzi, Gianni, Marco R. Oggioni, and Donata Medaglini. "Recombinant Streptococcus gordonii as a Live Vehicle for Vaccine Antigens." In Gram-Positive Bacteria, 35–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-07548-7_3.

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Andersen, Roxanna N., R. Dwayne Lunsford, and Paul E. Kolenbrander. "Determination of the Transcript Size and Start Site of the Putative sca Operon of Streptococcus gordonii ATCC 51656 (Formerly Strain PK488)." In Streptococci and the Host, 657–60. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1825-3_153.

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Obladen, Michael. "Systemic infection." In Oxford Textbook of the Newborn, edited by Michael Obladen, 345–50. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198854807.003.0049.

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In antiquity, transmission of disease was attributed to the miasma or contagion theory. In the Middle Ages, living in proximity to domestic animals and flies, the scarce use of soap, and absent sewage augmented the exposure to bacteria. In the early 19th century, Gordon, Holmes, and Semmelweis understood that maternal childbed fever—closely related to neonatal sepsis—was transferred by the physician’s hands to the mother during delivery. Before bacteria were discovered in the mid-19th century, septic infections in the newborn were perceived as different disorders: erysipelas, Buhl’s disease, Winckel’s disease, and so on. With the advent of microbiology, sepsis became heterogeneous and was mainly defined by the causing microorganism. In the 1940s, group B streptococci emerged as a pathogen of newborns and soon became the commonest cause of neonatal sepsis. The discovery of antibiotics made the deadly disease treatable. In the 1970s, resistant bacterial strains emerged and allied dangerously with indwelling devices, especially central venous catheters. In the developing world, neonatal sepsis remains a major cause of infant mortality.
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Conference papers on the topic "Streptococcus gordonii"

1

Bath, A. S., and J. Kaur. "A Rare Cause of Empyema: Streptococcus Gordonii." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a3727.

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Soekanto, Sri Angky, Saly Salim Alatas, Rima Ristanti, Ferry P. Gultom, and Muhamad Sahlan. "Efficacy of propolis fluoride in inhibiting the formation of Streptoccocus mutans, Streptococcus gordonii, and Streptococcus sanguinis biofilm." In SECOND INTERNATIONAL CONFERENCE OF MATHEMATICS (SICME2019). Author(s), 2019. http://dx.doi.org/10.1063/1.5096712.

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Withers, Nathan J., Arjun Senthil, Marek Osinski, Jane Q. Nguyen, Gema Alas, Christina Minetos, Nikita Jaiswal, Sergei A. Ivanov, Gennady A. Smolyakov, and Dale L. Huber. "Effects of iron-oxide nanoparticles on compound biofilms of streptococcus gordonii and fusobacterium nucleatum." In Colloidal Nanoparticles for Biomedical Applications XIII, edited by Xing-Jie Liang, Wolfgang J. Parak, and Marek Osiński. SPIE, 2018. http://dx.doi.org/10.1117/12.2299280.

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