Analysis of <i>Streptococcus mutans</i> biofilm proteins recognized by salivary immunoglobulin A

Sanui, Terukazu; Gregory, Richard L.

doi:10.1111/j.1399-302x.2009.00523.x

Cited by 22 publications

(9 citation statements)

References 33 publications

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“…The different results obtained, between that study and the present one, for treatment of S. mutans 10449 with 1.62 mg ml À1 of nicotine could be explained by the different concentrations of bacteria in the starting culture, which were approximately 10 3 -10 4 CFU ml À1 in the study of KEENE & JOHNSON (18) and 10 6 CFU ml À1 in the present study). Biofilms are the preferred form of growth for most bacteria (26), and protein expression in biofilm is different from protein expression in planktonic cells (27). The present study revealed that the nicotine-induced growth enhancement of planktonic cells is minor, because growth up-regulation was demonstrated only for A32-2 at nicotine concentrations of 0.25 and 0.5 mg ml À1 .…”

Section: Discussionmentioning

confidence: 54%

“…Biofilms are the preferred form of growth for most bacteria , and protein expression in biofilm is different from protein expression in planktonic cells . The present study revealed that the nicotine‐induced growth enhancement of planktonic cells is minor, because growth up‐regulation was demonstrated only for A32‐2 at nicotine concentrations of 0.25 and 0.5 mg ml −1 .…”

Section: Discussionmentioning

confidence: 59%

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Effect of nicotine on growth and metabolism of Streptococcus mutans

Huang

Gregory

2012

European J Oral Sciences

127

165

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Streptococcus mutans is a key contributor to dental caries. Smokers have a higher number of caries-affected teeth than do nonsmokers, but the association among tobacco, nicotine, caries, and S. mutans growth has not been investigated in detail. Seven S. mutans strains--UA159, UA130, 10449, A32-2, NG8, LM7, and OMZ175--were used in the present study. The minimum inhibitory concentration (MIC), minimum bactericidal concentration (MBC), minimum biofilm inhibitory concentration (MBIC), planktonic cell growth, biofilm formation, metabolism, and structure (determined using scanning electron microscopy) of the seven strains treated with different concentrations of nicotine (0-32 mg ml(-1)) were investigated. The MIC, MBC, and MBIC were 16 mg ml(-1) (0.1 M), 32 mg ml(-1) (0.2 M), and 16 mg ml(-1) (0.1 M), respectively, for most of the S. mutans strains. Growth of planktonic S. mutans cells was significantly repressed by 2.0-8.0 mg ml(-1) of nicotine. Biofilm formation and metabolic activity of S. mutans was increased in a nicotine-dependent manner up to 16.0 mg ml(-1) of nicotine. Scanning electron microscopy revealed that S. mutans treated with a high concentration of nicotine a had thicker biofilm and more spherical bacterial cells. In summary, nicotine enhances S. mutans biofilm formation and biofilm metabolic activity. These results suggest that smoking can increase the development of caries by fostering increased formation of S. mutans biofilm on tooth surfaces.

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Section: Discussionmentioning

confidence: 54%

Section: Discussionmentioning

confidence: 59%

Effect of nicotine on growth and metabolism of Streptococcus mutans

Huang

Gregory

2012

European J Oral Sciences

127

165

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“…Bacterial cells in biofilm acquire distinguishing characteristics compared to planktonic cells. Previous studies in our lab 24 demonstrated different protein expression in biofilm and planktonic S. mutans, in which fructan hydrolase, exo-beta-D-fructosidase, fructanase and cell division protein FtsG were enhanced in biofilm organisms compared to planktonic cells, but antigen I/II, glucosamine-fructose-6-phosphate aminotransferase I and chaperonin GroEL were repressed in biofilm cells. Some of our preliminary data indicate that in planktonic cells low concentrations of nicotine (0.25-0.5 mg/ml) enhanced S. mutans growth, while higher concentrations (2-4 mg/ml) of nicotine repressed S. mutans growth, but in biofilm both low and high concentrations of nicotine enhanced S. mutans growth (Huang, Li and Gregory, manuscript in preparation).…”

Section: Cooperation In Biofilmmentioning

confidence: 67%

Bacterial interactions in dental biofilm

2011

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“…2D-PAGE was used to separate the cellular proteins as previously described [25]. Prior to 2D-PAGE, contaminants including lipids, salts, and detergents were removed from the affinity-purified GST protein samples using ReadyPrep™ 2D Clean-Up Kit (Bio-Rad, Hercules, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

Identification of Novel Amelogenin-Binding Proteins by Proteomics Analysis

et al. 2013

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Emdogain (enamel matrix derivative, EMD) is well recognized in periodontology. It is used in periodontal surgery to regenerate cementum, periodontal ligament, and alveolar bone. However, the precise molecular mechanisms underlying periodontal regeneration are still unclear. In this study, we investigated the proteins bound to amelogenin, which are suggested to play a pivotal role in promoting periodontal tissue regeneration. To identify new molecules that interact with amelogenin and are involved in osteoblast activation, we employed coupling affinity chromatography with proteomic analysis in fractionated SaOS-2 osteoblastic cell lysate. In SaOS-2 cells, many of the amelogenin-interacting proteins in the cytoplasm were mainly cytoskeletal proteins and several chaperone molecules of heat shock protein 70 (HSP70) family. On the other hand, the proteomic profiles of amelogenin-interacting proteins in the membrane fraction of the cell extracts were quite different from those of the cytosolic-fraction. They were mainly endoplasmic reticulum (ER)-associated proteins, with lesser quantities of mitochondrial proteins and nucleoprotein. Among the identified amelogenin-interacting proteins, we validated the biological interaction of amelogenin with glucose-regulated protein 78 (Grp78/Bip), which was identified in both cytosolic and membrane-enriched fractions. Confocal co-localization experiment strongly suggested that Grp78/Bip could be an amelogenin receptor candidate. Further biological evaluations were examined by Grp78/Bip knockdown analysis with and without amelogenin. Within the limits of the present study, the interaction of amelogenin with Grp78/Bip contributed to cell proliferation, rather than correlate with the osteogenic differentiation in SaOS-2 cells. Although the biological significance of other interactions are not yet explored, these findings suggest that the differential effects of amelogenin-derived osteoblast activation could be of potential clinical significance for understanding the cellular and molecular bases of amelogenin-induced periodontal tissue regeneration.

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Analysis of Streptococcus mutans biofilm proteins recognized by salivary immunoglobulin A

Cited by 22 publications

References 33 publications

Effect of nicotine on growth and metabolism of Streptococcus mutans

Effect of nicotine on growth and metabolism of Streptococcus mutans

Bacterial interactions in dental biofilm

Identification of Novel Amelogenin-Binding Proteins by Proteomics Analysis

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