The impact of growth conditions on biofilm formation and the cell surface hydrophobicity in fluconazole susceptible and tolerant Candida albicans

2014 ◽  
Vol 60 (1) ◽  
pp. 45-51 ◽  
Author(s):  
Anna Kolecka ◽  
Dušan Chorvát ◽  
Helena Bujdáková
Microbiology ◽  
2004 ◽  
Vol 150 (2) ◽  
pp. 285-292 ◽  
Author(s):  
David R. Singleton ◽  
Kevin C. Hazen

Cell-surface hydrophobicity (CSH) in Candida albicans contributes to virulence and can be conveniently regulated in planktonic cultures by altering growth temperature. The CSH1 gene is the first candidate gene that has been demonstrated to play a role in affecting the CSH phenotype. However, the primary amino acid sequence of the CSH1 gene product suggests that the protein should be restricted to the cytoplasm. A majority of the protein appears to demonstrate that localization. Cell-surface biotinylation and limited glucanase digestion were used to determine and estimate the relative amount of Csh1p in the extracellular compartment in comparison to the cytoplasmic pool. Additionally, Western and Northern blotting were used to assess expression of the CSH1 gene under different growth conditions. Compared with cells grown at 23 °C, the total cellular levels of Csh1p are significantly greater at elevated growth temperatures. Detection of Csh1p on the cell surface correlates with the level of overall protein expression. The temperature-dependent regulation and surface presentation of Csh1p suggests a mechanism for regulating the CSH phenotype.


2005 ◽  
Vol 49 (2) ◽  
pp. 584-589 ◽  
Author(s):  
Ying-Ying Cao ◽  
Yong-Bing Cao ◽  
Zheng Xu ◽  
Kang Ying ◽  
Yao Li ◽  
...  

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.


2017 ◽  
Vol 14 (4) ◽  
pp. 1503-1511 ◽  
Author(s):  
Renuka R. Goswami ◽  
Suhas D. Pohare ◽  
Jayant S. Raut ◽  
S. Mohan Karuppayil

ABSTRACT: Cell surface hydrophobicity (CSH) is one of the important virulence attributes which helps Candida albicans to be a successful fungal pathogen. It influences several steps in pathogenesis of C. albicans leading to establishment of infection. CSH plays an important role in adhesion of cells to host tissues and catheters/medical devices implanted in patients. Adhesion to surfaces and subsequent biofilm formation are crucial because it may result in resistance to antifungal drugs. This important pathogenicity determinant would also be an attractive antifungal target. Various studies indicate that antifungal drugs tend to lower the CSH of Candida cells. Interestingly, molecules of plant origin have been reported to modulate CSH, reduce adhesion and interfere in biofilm formation by C. albicans. The review presents a brief account of biochemical basis of CSH, its role in adhesion and biofilm formation by C. albicans as well as explores it as an antifungal drug target.


2013 ◽  
Vol 8 (3) ◽  
pp. 259-262 ◽  
Author(s):  
Helena Bujdáková ◽  
Miroslava Didiášová ◽  
Hana Drahovská ◽  
Lucia Černáková

AbstractOverall cell surface hydrophobicity (CSH) is predicted to play an important role during biofilm formation in Candida albicans but is the result of many expressed proteins. This study compares the CSH status and CSH1 gene expression in C. albicans planktonic cells, sessile biofilm, and dispersal cells. Greater percentages of hydrophobic cells were found in non-adhered (1.5 h) and dispersal forms (24 or 48 h) (41.34±4.17% and 39.52±7.45%, respectively), compared with overnight planktonic cultures (21.69±3.60%). Results from quantitative real-time PCR confirmed greater up-regulation of the CSH1 gene in sessile biofilm compared with both planktonic culture and dispersal cells. Up-regulation was also greater in dispersal cells compared with planktonic culture. The markedly increased CSH found both in C. albicans biofilm, and in cells released during biofilm formation could provide an advantage to dispersing cells building new biofilm.


Author(s):  
Yi Wang ◽  
Lakshman P Samaranayake ◽  
Gary A Dykes

Abstract We hypothesized that the initial events leading to biofilm formation by bacteria, in general, are predominantly mediated by cell surface physicochemical interactions, and that natural products can impact the process by altering cell surface physicochemical properties. We exemplified this phenomenon using Actinomyces naeslundii as the model organism, and using tea products to modify its cell surface physicochemical properties. To test the hypothesis, a non-linear multiple regression model incorporating a normal distribution curve was constructed to explain the impact of tea extracts on the physiochemical processes of biofilm formation by A. naeslundii. The model utilized tea extract-induced changes in cell surface physicochemical properties as independent variables, and the corresponding biofilm formation as a dependent variable. Five different tea extracts were used to treat A. naeslundii, and their impact on the cell surface hydrophobicity, charge, auto-aggregation, attachment and biofilm formation on four different hard surfaces were measured and the data were used to construct the model. The established model was then tested in independent experiments involving other plant extracts and purified phytochemicals. Experimental results showed that the tea extracts significantly reduced cell surface hydrophobicity (by up to 21.3%), increased cell surface charge and auto-aggregation (by up to 4.5 mV and 14.9%, respectively), inhibited attachment (by 0.6–2.5 log CFU cm−2) and affected biofilm formation (by up to 0.6 log CFU cm−2). The model indicated that both cell surface hydrophobicity and charge played an important role in bacterial auto-aggregation and attachment, and that the latter two phenomena significantly correlated with subsequent biofilm development. The accuracy of the model construct was approximately 64%. This modelling approach can be employed for other microbial colonization systems to predict biofilm formation, and to study the impact of cell surface physicochemical properties in biofilm development.


Molecules ◽  
2018 ◽  
Vol 23 (10) ◽  
pp. 2418 ◽  
Author(s):  
Luanda Souza ◽  
Walicyranison Silva-Rocha ◽  
Magda Ferreira ◽  
Luiz Soares ◽  
Terezinha Svidzinski ◽  
...  

This study evaluated the influence of the extract of Eugenia uniflora in adhesion to human buccal epithelial cells (HBEC) biofilm formation and cell surface hydrophobicity (CSH) of Candida spp. isolated from the oral cavity of kidney transplant patients. To evaluate virulence attributes in vitro, nine yeasts were grown in the presence and absence of 1000 μg/mL of the extract. Adhesion was quantified using the number of Candida cells adhered to 150 HBEC determined by optical microscope. Biofilm formation was evaluated using two methodologies: XTT (2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide) and crystal violet assay, and further analyzed by electronic scan microscopy. CSH was quantified with the microbial adhesion to hydrocarbons test. We could detect that the extract of E. uniflora was able to reduce adhesion to HBEC and CSH for both Candida albicans and non-Candida albicans Candida species. We also observed a statistically significant reduced ability to form biofilms in biofilm-producing strains using both methods of quantification. However, two highly biofilm-producing strains of Candida tropicalis had a very large reduction in biofilm formation. This study reinforces the idea that besides growth inhibition, E. uniflora may interfere with the expression of some virulence factors of Candida spp. and may be possibly applied in the future as a novel antifungal agent.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Engy A. Elekhnawy ◽  
Fatma I. Sonbol ◽  
Tarek E. Elbanna ◽  
Ahmed A. Abdelaziz

Abstract Background The percentage of the multidrug resistant Klebsiella pneumoniae clinical isolates is increasing worldwide. The excessive exposure of K. pneumoniae isolates to sublethal concentrations of biocides like benzalkonium chloride (BAC) in health care settings and communities could be one of the causes contributing in the global spread of antibiotic resistance. Results We collected 50 K. pneumoniae isolates and these isolates were daily exposed to gradually increasing sublethal concentrations of BAC. The consequence of adaptation to BAC on the cell surface hydrophobicity (CSH) and biofilm formation of K. pneumoniae isolates was explored. Remarkably, 16% of the tested isolates showed an increase in the cell surface hydrophobicity and 26% displayed an enhanced biofilm formation. To evaluate whether the influence of BAC adaptation on the biofilm formation was demonstrated at the transcriptional level, the RT-PCR was employed. Noteworthy, we found that 60% of the tested isolates exhibited an overexpression of the biofilm gene (bssS). After sequencing of this gene in K. pneumoniae isolates before and after BAC adaptation and performing pairwise alignment, 100% identity was detected; a finding that means the absence of mutation after adaptation to BAC. Conclusion This study suggests that the widespread and increased use of biocides like BAC at sublethal concentrations has led to an increase biofilm formation by K. pneumoniae isolates. Enhanced biofilm formation could result in treatment failure of the infections generated by this pathogen.


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