scholarly journals Effects of fluconazole treatment of mice infected with fluconazole-susceptible and -resistant Candida tropicalis on fungal cell surface hydrophobicity, adhesion and biofilm formation

2015 ◽  
Vol 33 (5) ◽  
pp. 97 ◽  
Author(s):  
SF Yamada-Ogatta ◽  
RL Kanoshiki ◽  
SB de Paula ◽  
JP Santos ◽  
AT Morey ◽  
...  
Keyword(s):  
Cell Surface ◽  
Candida Tropicalis ◽  
Biofilm Formation ◽  
Cell Surface Hydrophobicity ◽  
Surface Hydrophobicity ◽  
Fungal Cell

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 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 Virulence Factors and Azole-Resistant Mechanism of Candida Tropicalis Isolated From Candidemia

2021 ◽  
Author(s):  
Elahe Sasani ◽  
Sadegh Khodavaisy ◽  
Sassan Rezaie ◽  
Mohammadreza Salehi ◽  
Muhammad Getso ◽  
...  
Keyword(s):  
Virulence Factors ◽  
Candida Tropicalis ◽  
Biofilm Formation ◽  
Molecular Mechanisms ◽  
Antifungal Susceptibility ◽  
Cell Surface Hydrophobicity ◽  
Surface Hydrophobicity ◽  
Azole Resistance ◽  
Virulence Determinants ◽  
Fluconazole Resistant

Abstract Background Virulence factors intensify the pathogenicity of Candida species in candidemia. Limited knowledge exists regarding the azole-resistant mechanism and virulence factors of Candida tropicalis. Consequently, we aimed to evaluate the virulence factors and the molecular mechanisms of azole resistance among C. tropicalis isolated from bloodstream infection. Materials and methods Forty-five C. tropicalis isolates recovered from candidemia patients were evaluated for virulence factors, including extracellular enzymatic activities, cell surface hydrophobicity (CHS), and biofilm formation. Antifungal susceptibility pattern and expression level of ERG11, UPC2, MDR1, and CDR1 genes of eight azole resistance C. tropicalis isolates were assessed. Results The isolates expressed different frequencies of virulence determinants as follows: coagulase 4 (8.9%), phospholipase 4 (8.9 %), proteinase 31 (68.9 %), CSH 43 (95.6 %), esterase 43 (95.6 %), hemolysin 44 (97.8%), and biofilm formation 45 (100%). All the isolates were susceptible to amphotericin B and showed the highest resistance to voriconazole. The high expression of ERG11 and UPC2 genes in fluconazole-resistant C. tropicalis isolates were observed. Conclusion C. tropicalis isolated from candidemia patients extensively displayed capacities for biofilm formation, hemolysis, esterase activity, and hydrophobicity. In addition, the overexpression of ERG11 and UPC2 genes can be considered as one of the possible mechanisms of azole resistance.

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.

Sign in / Sign up

Export Citation Format

Share Document