Invasion of human coronary artery endothelial cells by <i>Streptococcus mutans</i> OMZ175

Abranches, Jacqueline; Zeng, Lin; Bélanger, Myriam; Rodrigues, Paulo Henrique Mazza; Simpson-Haidaris, Patricia J.; Akin, Debra; Dunn, William A.; Progulske‐Fox, Ann; Burne, Robert A.

doi:10.1111/j.1399-302x.2008.00487.x

Cited by 75 publications

(81 citation statements)

References 29 publications

(41 reference statements)

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“…Because there was a strong correlation between non-serotype c strains and HCAEC invasion, we hypothesized that cnm plays a role in cellular invasion by S. mutans. Indeed, we found that of the 33 S. mutans strains tested in the present study and a previous study (2), only the 5 invasive strains harbored a copy of the cnm gene (Fig. 3A).…”

Section: Resultsmentioning

confidence: 61%

“…In a previous study, strains B14 and OMZ175, belonging to serotypes e and f, respectively, were able to invade HCAEC, whereas none of the 8 serotype c strains tested displayed invasive behavior (2). To increase the number of serotype e and f strains screened, we assessed the capacity of 19 additional strains to invade HCAEC: 12 isolated from the blood of patients with bacteremia and/or IE (10 serotype c, 1 serotype e, and 1 serotype f strain) and 7 isolated from dental plaque (1 serotype c, 4 serotype e, and 2 serotype f strains).…”

Section: Resultsmentioning

confidence: 99%

“…All strains listed in Table 1 and those from a previous study (2) were assessed for the presence of the cnm gene by PCR using the primers cnm-1F and cnm-1R (43,54). Cnm ϩ strains had the cnm gene disrupted by insertion of a nonpolar kanamycin marker (28) 700 bp downstream of the ATG start codon, using a PCR-ligation mutagenesis strategy (30).…”

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confidence: 99%

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The Collagen-Binding Protein Cnm Is Required for Streptococcus mutans Adherence to and Intracellular Invasion of Human Coronary Artery Endothelial Cells

et al. 2011

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Streptococcus mutans is considered the primary etiologic agent of dental caries, a global health problem that affects 60 to 90% of the population, and a leading causative agent of infective endocarditis. It can be divided into four different serotypes (c, e, f, and k), with serotype c strains being the most common in the oral cavity. In this study, we demonstrate that in addition to OMZ175 and B14, three other strains (NCTC11060, LM7, and OM50E) of the less prevalent serotypes e and f are able to invade primary human coronary artery endothelial cells (HCAEC). Invasive strains were also significantly more virulent than noninvasive strains in the Galleria mellonella (greater wax worm) model of systemic disease. Interestingly, the invasive strains carried an additional gene, cnm, which was previously shown to bind to collagen and laminin in vitro. Inactivation of cnm rendered the organisms unable to invade HCAEC and attenuated their virulence in G. mellonella. Notably, the cnm knockout strains did not adhere to HCAEC as efficiently as the parental strains did, indicating that the loss of the invasion phenotype observed for the mutants was linked to an adhesion defect. Comparisons of the invasive strains and their respective cnm mutants did not support a correlation between biofilm formation and invasion. Thus, Cnm is required for S. mutans invasion of endothelial cells and possibly represents an important virulence factor of S. mutans that may contribute to cardiovascular infections and pathologies.

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Section: Resultsmentioning

confidence: 61%

Section: Resultsmentioning

confidence: 99%

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The Collagen-Binding Protein Cnm Is Required for Streptococcus mutans Adherence to and Intracellular Invasion of Human Coronary Artery Endothelial Cells

et al. 2011

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“…The survival ability within human cells has been previously shown only for S. mutans (17), while no data is available for S. sobrinus. Not tending to adhesion and invasion efficiencies, S. mutans and S. sobrinus biofilm did not show higher survival efficiency than planktonic bacteria even if different values were observed.…”

Section: Discussionmentioning

confidence: 99%

Streptococcus Mutans and Streptococcus Sobrinus are Able to Adhere and Invade Human Gingival Fibroblast Cell Line

Berlutti

Catizone

Ricci

et al. 2010

Int J Immunopathol Pharmacol

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Streptococcus mutans and Streptococcus sobrinus, the principal etiologic agents of caries decay of teeth, are generally acquired in oral cavity at the moment of tooth eruption. However, as S. mutans has been detected in oral cavity of predentate children, the eruption of teeth seems not to be a necessary prerequisite, suggesting that this species may be not confined to dental plaque. Here, we evaluate the ability of S. mutans and S. sobrinus in planktonic and biofilm lifestyle to adhere, invade and survive within human gingival fibroblast (HGF-l) cells. Planktonic and biofilm streptococci adhered and invaded host cells to different extents, showing higher efficiencies of biofilm than planktonic counterparts. Moreover, planktonic and biofilm streptococci showed the same percentage of survival within host cells. Transmission electron and confocal microscopy observations confirmed intracellular localization of planktonic and biofilm bacteria. The adhesion, invasion and survival abilities within human oral cells may be considered S. mutans and S. sobrinus virulence mechanisms to colonize and persist in the oral cavity in the absence of tooth surface.Streptococcus mutans and S. sobrinus belonging to the phylogenetic mutans group (1) are considered the principal etiologic agents of caries decay of teeth . (2-4). These bacterial species are characterized by common virulence factors, including the adhesion and colonization ability of teeth surfaces by sucroseindependent and sucrose-dependent mechanisms (6-8). Sucrose availability induces the up-expression of biofilm-associated genes thus promoting biofilm development on tooth surfaces (9-10). The biofilm lifestyle increases streptococcal resistance against antimicrobial substances allowing the survival and persistence in oral cavity (11)(12).Studies on timing of acquisition have shown that S. mutans and S. sobrinus can be acquired at any time from 6 months to over 3 years of age, corresponding to the eruption of teeth as they require a nonshedding surface to adhere, colonize and multiply (4-5, 13). However, tooth eruption seems not to be a necessary prerequisite for mutans streptococci

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“…mutans strain OMZ175 was used in this study and was cultured and maintained for infection of mice as described previously (Abranches et al, 2009). The concentration of bacteria was determined quantitatively, and the organism was re-suspended in phosphate-buffered saline (pH 7.2) at 1 x 10 9 bacteria per mL.…”

Section: Materials and Methods Bacterial Strain And Microbial Inoculamentioning

confidence: 99%

Increased Atherogenesis during Streptococcus mutans Infection in ApoE-null Mice

et al. 2012

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A supplemental appendix to this article is published electronically only at http://jdr.sagepub.com/supplemental. AbstrAct Streptococcus mutans, a dental caries pathogen, also causes endocarditis and is detected in atheroscelerotic plaque. We investigated the potential for an invasive strain of S. mutans, OMZ175, to accelerate plaque growth in apolipoprotein E deficient (ApoE null ) mice without and with balloon angioplasty (BA) injury, a model of restenosis. ApoE null mice were divided into 4 groups (N = 10), 2 with and 2 without BA. One each of the BA and non-BA groups was infected with S. mutans (Sm). S. mutans DNA, plaque area, inflammatory cell invasion, and Toll-like receptor (TLR) expression were measured at 6-20 weeks post-infection. S. mutans genomic DNA was detected in the aorta, liver, spleen, and heart. Plaque growth was significantly increased in infected mice with BA (Sm+BA) vs. those in the non-infected groups (p < 0.03). Plaque size was increased after infection without BA (Sm), but did not reach significance. Aortic specimens from both S. mutans and Sm+BA groups displayed increased numbers of macrophages, and TLR4 expression was increased in BA mice. In conclusion, S. mutans infection accelerated plaque growth, macrophage invasion, and TLR4 expression after angioplasty. S. mutans may also be associated with atherosclerotic plaque growth in non-injured arteries.

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Invasion of human coronary artery endothelial cells by Streptococcus mutans OMZ175

Cited by 75 publications

References 29 publications

The Collagen-Binding Protein Cnm Is Required for Streptococcus mutans Adherence to and Intracellular Invasion of Human Coronary Artery Endothelial Cells

The Collagen-Binding Protein Cnm Is Required for Streptococcus mutans Adherence to and Intracellular Invasion of Human Coronary Artery Endothelial Cells

Streptococcus Mutans and Streptococcus Sobrinus are Able to Adhere and Invade Human Gingival Fibroblast Cell Line

Increased Atherogenesis during Streptococcus mutans Infection in ApoE-null Mice

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