Streptococcus mutans and cardiovascular diseases

Nakano, Kazuhiko; Nomura, Ryota; Ooshima, Takashi

doi:10.1016/j.jdsr.2007.09.001

Cited by 34 publications

(36 citation statements)

References 91 publications

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“…In addition, S. mutans can cause extra‐oral infections such as infective endocarditis (Mylonakis & Calderwood, ; Nagata et al ., ; Nakano et al ., ) and has been proposed to participate in the development of atherosclerosis (Nakano et al ., ; Kesavalu et al ., ). Strains of S. mutans are classified in four serotypes ( c , e , f and k ) based on the chemical composition of the cell surface rhamnose–glucose polysaccharide (Nakano et al ., , ). In clinical samples, ~ 70% of S. mutans isolates from dental plaque belong to serotype c and nearly 20% to serotype e , while serotypes f and k comprise less than 5% each (Nakano et al ., ,b, ).…”

Section: Introductionmentioning

confidence: 99%

“…Strains of S. mutans are classified in four serotypes ( c , e , f and k ) based on the chemical composition of the cell surface rhamnose–glucose polysaccharide (Nakano et al ., , ). In clinical samples, ~ 70% of S. mutans isolates from dental plaque belong to serotype c and nearly 20% to serotype e , while serotypes f and k comprise less than 5% each (Nakano et al ., ,b, ). Despite its well‐established association in blood‐borne infections, the mechanisms associated with S. mutans infection and persistence in extra‐oral sites are still poorly understood.…”

Section: Introductionmentioning

confidence: 99%

“…A major contributor in the development of dental caries, Streptococcus mutans has been the subject of extensive research and the mechanisms associated with its ability to colonize and thrive in the oral environment have been well documented (Loesche, 1986;Bowen & Koo, 2011). In addition, S. mutans can cause extra-oral infections such as infective endocarditis (Mylonakis & Calderwood, 2001;Nagata et al, 2006;Nakano et al, 2008) and has been proposed to participate in the development of atherosclerosis (Nakano et al, 2006;Kesavalu et al, 2012). Strains of S. mutans are classified in four serotypes (c, e, f and k) based on the chemical composition of the cell surface rhamnose-glucose polysaccharide (Nakano et al, 2007a(Nakano et al, , 2008.…”

Section: Introductionmentioning

confidence: 99%

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Cnm is a major virulence factor of invasive Streptococcus mutans and part of a conserved three‐gene locus

Avilés‐Reyes

Miller

Simpson-Haidaris

et al. 2014

Molecular Oral Microbiology

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Cnm, a collagen- and laminin-binding protein present in a subset of Streptococcus mutans strains, mediates binding to extracellular matrices (ECM), intracellular invasion and virulence in the Galleria mellonella model. Antibodies raised against Cnm were used to confirm expression and the cell surface localization of Cnm in the highly invasive OMZ175 strain. Sequence analysis identified two additional genes (cnaB and cbpA) encoding putative surface proteins immediately upstream of cnm. Inactivation of cnaB and cbpA in OMZ175, individually or in combination, did not decrease the ability of this highly invasive and virulent strain to bind to different ECM proteins, invade human coronary artery endothelial cells (HCAEC), or kill G. mellonella. Similarly, expression of cnaB and cbpA in the cnm(-) strain UA159 revealed that these genes did not enhance Cnm-related phenotypes. However, integration of cnm in the chromosome of UA159 significantly increased its ability to bind to collagen and laminin, invade HCAEC, and kill G. mellonella. Moreover, the presence of antibodies against Cnm nearly abolished the ability of OMZ175 to bind to collagen and laminin and invade HCAEC, and significantly protected G. mellonella against OMZ175 infection. We concluded that neither CnaB nor CbpA is necessary for the expression of Cnm-related traits. We also provided definitive evidence that Cnm is an important virulence factor and a suitable target for the development of novel preventive and therapeutic strategies to combat invasive S. mutans strains.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cnm is a major virulence factor of invasive Streptococcus mutans and part of a conserved three‐gene locus

Avilés‐Reyes

Miller

Simpson-Haidaris

et al. 2014

Molecular Oral Microbiology

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“…Strains of S. mutans are classified in four serotypes (c, e, f, and k), with approximately 70% of strains isolated from dental plaque belonging to serotype c, over 20% belonging to serotype e, and less than 5% belonging to serotypes f and k (3,4). In addition to dental caries, S. mutans is frequently associated with nonoral diseases, such as infective endocarditis (IE) and, possibly, atherosclerotic coronary heart diseases (ACHD) (5,6). Combined, staphylococci, enterococci, and viridans group streptococci are responsible for more than 80% of all cases of IE, and it is estimated that S. mutans is responsible for ϳ20% of cases caused by viridans group streptococci (7,8).…”

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confidence: 99%

Modification of Streptococcus mutans Cnm by PgfS Contributes to Adhesion, Endothelial Cell Invasion, and Virulence

et al. 2014

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Expression of the surface protein Cnm has been directly implicated in the ability of certain strains of Streptococcus mutans to bind to collagen and to invade human coronary artery endothelial cells (HCAEC) and in the killing of Galleria mellonella. Sequencing analysis of Cnm ؉ strains revealed that cnm is located between the core genes SMU.2067 and SMU.2069. Reverse transcription-PCR (RT-PCR) analysis showed that cnm is cotranscribed with SMU.2067, encoding a putative glycosyltransferase referred to here as PgfS (protein glycosyltransferase of streptococci). Notably, Cnm contains a threonine-rich domain predicted to undergo O-linked glycosylation. The previously shown abnormal migration pattern of Cnm, the presence of the threonine-rich domain, and the molecular linkage of cnm with pgfS lead us to hypothesize that PgfS modifies Cnm. A ⌬pgfS strain showed defects in several traits associated with Cnm expression, including collagen binding, HCAEC invasion, and killing of G. mellonella. Western blot analysis revealed that Cnm from the ⌬pgfS mutant migrated at a lower molecular weight than that from the parent strain. In addition, Cnm produced by ⌬pgfS was highly susceptible to proteinase K degradation, in contrast to the high-molecular-weight Cnm version found in the parent strain. Lectin-binding analyses confirmed the glycosylated nature of Cnm and strongly suggested the presence of N-acetylglucosamine residues attached to Cnm. Based on these findings, the phenotypes observed in ⌬pgfS are most likely associated with defects in Cnm glycosylation that affects protein function, stability, or both. In conclusion, this study demonstrates that Cnm is a glycoprotein and that posttranslational modification mediated by PgfS contributes to the virulence-associated phenotypes linked to Cnm.

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“…Serotype-specific antisera used in studies of S. mutans are conventionally generated by intramuscular immunization of whole cells into rabbits twice over a period of 1 week, which is a relatively easy procedure (16). However, we were unable to generate antisera for TW295 and TW871 by that usual method, which was considered to be caused by their lower antigenicity due to the lack of glucose side-chains in the serotype-specific polysaccharides.…”

Section: Non-c/e/f Serotype Strains Isolated From Human Bloodmentioning

confidence: 99%

Roles of Oral Bacteria in Cardiovascular Diseases — From Molecular Mechanisms to Clinical Cases: Cell-Surface Structures of Novel Serotype k Streptococcus mutans Strains and Their Correlation to Virulence

et al. 2010

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Abstract. Streptococcus mutans is generally known as a pathogen of dental caries, and it is also considered to cause bacteremia and infective endocarditis (IE). S. mutans was previously classified into 3 serotypes, c, e, and f , due to the different chemical compositions of the serotype-specific polysaccharides, which are composed of a rhamnose backbone and glucose side chains. We recently designated non-c / e / f serotype S. mutans strains as novel serotype k , which is characterized by a drastic reduction in the amount of the glucose side chain. A common biological feature of novel serotype-k strains is a lower level of cariogenicity due to alterations of several major cell surface protein antigens. As for virulence in blood, these strains survive in blood for a longer duration due to lower antigenicity, while the detection rate of all strains carrying the gene encoding collagen-binding adhesin has been shown to be high. Furthermore, molecular biological analyses of infected heart valve specimens obtained from IE patients revealed a high detection rate of serotype-k S. mutans . Together, these findings suggest that serotype-k S. mutans strains show low cariogenicity but high virulence in blood as compared to the other serotypes, due to alterations of several cell surface structures.

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Streptococcus mutans and cardiovascular diseases

Cited by 34 publications

References 91 publications

Cnm is a major virulence factor of invasive Streptococcus mutans and part of a conserved three‐gene locus

Cnm is a major virulence factor of invasive Streptococcus mutans and part of a conserved three‐gene locus

Modification of Streptococcus mutans Cnm by PgfS Contributes to Adhesion, Endothelial Cell Invasion, and Virulence

Roles of Oral Bacteria in Cardiovascular Diseases — From Molecular Mechanisms to Clinical Cases: Cell-Surface Structures of Novel Serotype k Streptococcus mutans Strains and Their Correlation to Virulence

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