Cell surface hydrophobicity, biofilm formation, adhesives properties and molecular detection of adhesins genes in Staphylococcus aureus associated to dental caries

2010 ◽  
Vol 49 (1-2) ◽  
pp. 14-22 ◽  
Author(s):  
Bochra Kouidhi ◽  
Tarek Zmantar ◽  
Hajer Hentati ◽  
Amina Bakhrouf
Keyword(s):  
Staphylococcus Aureus ◽  
Dental Caries ◽  
Cell Surface ◽  
Biofilm Formation ◽  
Molecular Detection ◽  
Cell Surface Hydrophobicity ◽  
Surface Hydrophobicity

scholarly journals Quercetin inhibits virulence properties of Porphyromas gingivalis in periodontal disease

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Zhiyan He ◽  
Xu Zhang ◽  
Zhongchen Song ◽  
Lu Li ◽  
Haishuang Chang ◽  
...  
Keyword(s):  
Cell Surface ◽  
Periodontal Disease ◽  
Biofilm Formation ◽  
Cell Structure ◽  
Cell Surface Hydrophobicity ◽  
Surface Hydrophobicity ◽  
Laser Scanning Microscopy ◽  
Confocal Laser ◽  
Antimicrobial Effects ◽  
Virulence Properties

Abstract Porphyromonas gingivalis is a causative agent in the onset and progression of periodontal disease. This study aims to investigate the effects of quercetin, a natural plant product, on P. gingivalis virulence properties including gingipain, haemagglutinin and biofilm formation. Antimicrobial effects and morphological changes of quercetin on P. gingivalis were detected. The effects of quercetin on gingipains activities and hemolytic, hemagglutination activities were evaluated using chromogenic peptides and sheep erythrocytes. The biofilm biomass and metabolism with different concentrations of quercetin were assessed by the crystal violet and MTT assay. The structures and thickness of the biofilms were observed by confocal laser scanning microscopy. Bacterial cell surface properties including cell surface hydrophobicity and aggregation were also evaluated. The mRNA expression of virulence and iron/heme utilization was assessed using real time-PCR. Quercetin exhibited antimicrobial effects and damaged the cell structure. Quercetin can inhibit gingipains, hemolytic, hemagglutination activities and biofilm formation at sub-MIC concentrations. Molecular docking analysis further indicated that quercetin can interact with gingipains. The biofilm became sparser and thinner after quercetin treatment. Quercetin also modulate cell surface hydrophobicity and aggregation. Expression of the genes tested was down-regulated in the presence of quercetin. In conclusion, our study demonstrated that quercetin inhibited various virulence factors of P. gingivalis.

scholarly journals Baicalein Inhibits Streptococcus mutans Biofilms and Dental Caries-Related Virulence Phenotypes

Antibiotics ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 215
Author(s):  
Aparna Vijayakumar ◽  
Hema Bhagavathi Sarveswari ◽  
Sahana Vasudevan ◽  
Karthi Shanmugam ◽  
Adline Princy Solomon ◽  
...  
Keyword(s):  
Dental Caries ◽  
Streptococcus Mutans ◽  
Biofilm Formation ◽  
Acid Production ◽  
Cell Surface Hydrophobicity ◽  
Surface Hydrophobicity ◽  
Oral Disease ◽  
Public Healthcare ◽  
Surface Attachment ◽  
First Time

Dental caries, the most common oral disease, is a major public healthcare burden and affects more than three billion people worldwide. The contemporary understanding of the need for a healthy microbiome and the emergence of antimicrobial resistance has resulted in an urgent need to identify compounds that curb the virulence of pathobionts without microbial killing. Through this study, we have demonstrated for the first time that 5,6,7-trihydroxyflavone (Baicalein) significantly downregulates crucial caries-related virulence phenotypes in Streptococcus mutans. Baicalein significantly inhibited biofilm formation by Streptococcus mutans UA159 (MBIC50 = 200 μM), without significant growth inhibition. Notably, these concentrations of baicalein did not affect the commensal S. gordonii. Strikingly, baicalein significantly reduced cell surface hydrophobicity, autoaggregation and acid production by S. mutans. Mechanistic studies (qRT-PCR) showed downregulation of various genes regulating biofilm formation, surface attachment, quorum sensing, acid production and competence. Finally, we demonstrate the potential translational value of baicalein by reporting synergistic interaction with fluoride against S. mutans biofilms.

scholarly journals Effect of Eugenol on Cell Surface Hydrophobicity, Adhesion, and Biofilm ofCandida tropicalisandCandida dubliniensisIsolated from Oral Cavity of HIV-Infected Patients

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Suelen Balero de Paula ◽  
Thais Fernanda Bartelli ◽  
Vanessa Di Raimo ◽  
Jussevania Pereira Santos ◽  
Alexandre Tadachi Morey ◽  
...  
Keyword(s):  
Cell Surface ◽  
Oral Cavity ◽  
Biofilm Formation ◽  
Cell Surface Hydrophobicity ◽  
Surface Hydrophobicity ◽  
Planktonic Cells ◽  
Hydrophobic Behavior ◽  
Significant Difference ◽  
Substrate Surfaces ◽  
Sessile Cells

MostCandidaspp. infections are associated with biofilm formation on host surfaces. Cells within these communities display a phenotype resistant to antimicrobials and host defenses, so biofilm-associated infections are difficult to treat, representing a source of reinfections. The present study evaluated the effect of eugenol on the adherence properties and biofilm formation capacity ofCandida dubliniensisandCandida tropicalisisolated from the oral cavity of HIV-infected patients. All isolates were able to form biofilms on different substrate surfaces. Eugenol showed inhibitory activity against planktonic and sessile cells ofCandidaspp. No metabolic activity in biofilm was detected after 24 h of treatment. Scanning electron microscopy demonstrated that eugenol drastically reduced the number of sessile cells on denture material surfaces. MostCandidaspecies showed hydrophobic behavior and a significant difference in cell surface hydrophobicity was observed after exposure of planktonic cells to eugenol for 1 h. Eugenol also caused a significant reduction in adhesion of mostCandidaspp. to HEp-2 cells and to polystyrene. These findings corroborate the effectiveness of eugenol againstCandidaspecies other thanC. albicans, reinforcing its potential as an antifungal applied to limit both the growth of planktonic cells and biofilm formation on different surfaces.

scholarly journals Factors associated with adherence to and biofilm formation on polystyrene byStenotrophomonas maltophilia: the role of cell surface hydrophobicity and motility

2008 ◽  
Vol 287 (1) ◽  
pp. 41-47 ◽  
Author(s):  
Arianna Pompilio ◽  
Raffaele Piccolomini ◽  
Carla Picciani ◽  
Domenico D'Antonio ◽  
Vincenzo Savini ◽  
...  
Keyword(s):  
Cell Surface ◽  
Biofilm Formation ◽  
Cell Surface Hydrophobicity ◽  
Surface Hydrophobicity ◽  
Factors Associated

scholarly journals Biofilm Formation and Cell Surface Properties among Pathogenic and Nonpathogenic Strains of the Bacillus cereus Group

2009 ◽  
Vol 75 (20) ◽  
pp. 6616-6618 ◽  
Author(s):  
Sandrine Auger ◽  
Nalini Ramarao ◽  
Christine Faille ◽  
Agnès Fouet ◽  
Stéphane Aymerich ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cell Surface ◽  
Bacillus Cereus ◽  
Digestive Tract ◽  
Biofilm Formation ◽  
Cell Surface Hydrophobicity ◽  
Surface Hydrophobicity ◽  
Bacillus Cereus Group ◽  
Cell Surface Properties ◽  
Tract Infections

ABSTRACT Biofilm formation by 102 Bacillus cereus and B. thuringiensis strains was determined. Strains isolated from soil or involved in digestive tract infections were efficient biofilm formers, whereas strains isolated from other diseases were poor biofilm formers. Cell surface hydrophobicity, the presence of an S layer, and adhesion to epithelial cells were also examined.

scholarly journals Inhibitory Effect ofBacillus velezensison Biofilm Formation byStreptococcus mutans

2018 ◽  
Author(s):  
Yesol Yoo ◽  
Dong-Ho Seo ◽  
Hyunjin Lee ◽  
Young-Do Nam ◽  
Myung-Ji Seo
Keyword(s):  
Dental Caries ◽  
Streptococcus Mutans ◽  
Biofilm Formation ◽  
Culture Medium ◽  
Focal Point ◽  
Cell Surface Hydrophobicity ◽  
Surface Hydrophobicity ◽  
Inhibitory Effect ◽  
Fermented Foods ◽  
Bacillus Velezensis

ABSTRACTStreptococcus mutansplays a key role in the development of dental caries and promotes the formation of oral biofilm produced by glucosyltransferases (GTFs).Bacillus velezensisK68 was isolated from traditional fermented foods and inhibits biofilm formation mediated byS. mutans. Gene amplification results demonstrated thatB. velezensisK68 contained genes for the biosynthesis of 1-deoxynojirimycin (1-DNJ), a known GTF expression inhibitor. The presence of the GabT1, Yktc1, and GutB1 genes required for 1-DNJ synthesis inB. velezensisK68 was confirmed. Supernatant fromB. velezensisK68 culture medium inhibited biofilm formation by 84% whenS. mutanswas cultured for 48 h, and inhibited it maximally when 1% glucose was added to theS. mutansculture medium as a GTF substrate. In addition, supernatant fromB. velezensisK68 medium containing 3 ppb 1- DNJ decreasedS. mutanscell surface hydrophobicity by 79.0 ± 0.8% compared with that of untreated control. The supernatant containing 1-DNJ decreasedS. mutansadherence by 99.97% and 98.83% under sugar-dependent and sugar-independent conditions, respectively.S. mutanstreated with the supernatant exhibited significantly reduced expression of the essential GTF genesgtfB,gtfC,andgtfDcompared to that in the untreated group. Thus,B. velezensisinhibits the biofilm formation, adhesion, and GTF gene expression ofS. mutansthrough 1- DNJ production.IMPORTANCEDental caries is among the most common infectious diseases worldwide, and its development is closely associated with physiological factors of bacteria, such as the biofilm formation and glucosyltransferase production ofStreptococcus mutans.Biofilms are difficult to remove once they have formed due to the exopolysaccharide matrix produced by the microorganisms residing in them; thus, inhibiting biofilm formation is a current focal point of research into prevention of dental caries. This study describes the inhibitory properties ofBacillus velezensisK68, an organism isolated from traditional Korean fermented foods, against biofilm formation byS. mutans. Herein, we show thatB. velezensisinhibits the biofilm formation, adherence to surfaces, and glucosyltransferase production ofS. mutans.

scholarly journals cDNA Microarray Analysis of Differential Gene Expression in Candida albicans Biofilm Exposed to Farnesol

2005 ◽  
Vol 49 (2) ◽  
pp. 584-589 ◽  
Author(s):  
Ying-Ying Cao ◽  
Yong-Bing Cao ◽  
Zheng Xu ◽  
Kang Ying ◽  
Yao Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Drug Resistance ◽  
Candida Albicans ◽  
Cell Surface ◽  
Microarray Analysis ◽  
Biofilm Formation ◽  
Cell Surface Hydrophobicity ◽  
Surface Hydrophobicity ◽  
Cdna Microarray Analysis ◽  
Hyphal Formation

ABSTRACT Candida albicans biofilms are structured microbial communities with high levels of drug resistance. Farnesol, a quorum-sensing molecule that inhibits hyphal formation in C. albicans, has been found to prevent biofilm formation by C. albicans. There is limited information, however, about the molecular mechanism of farnesol against biofilm formation. We used cDNA microarray analysis to identify the changes in the gene expression profile of a C. albicans biofilm inhibited by farnesol. Confocal scanning laser microscopy was used to visualize and confirm normal and farnesol-inhibited biofilms. A total of 274 genes were identified as responsive, with 104 genes up-regulated and 170 genes down-regulated. Independent reverse transcription-PCR analysis was used to confirm the important changes detected by microarray analysis. In addition to hyphal formation-associated genes (e.g., TUP1, CRK1, and PDE2), a number of other genes with roles related to drug resistance (e.g., FCR1 and PDR16), cell wall maintenance (e.g., CHT2 and CHT3), and iron transport (e.g., FTR2) were responsive, as were several genes encoding heat shock proteins (e.g., HSP70, HSP90, HSP104, CaMSI3, and SSA2). Further study of these differentially regulated genes is warranted to evaluate how they may be involved in C. albicans biofilm formation. Consistent with the down-regulation of the cell surface hydrophobicity-associated gene (CSH1), the water-hydrocarbon two-phase assay showed a decrease in cell surface hydrophobicity in the farnesol-treated group compared to that in the control group. Our data provide new insight into the molecular mechanism of farnesol against C. albicans biofilm formation.

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