scholarly journals Divergent Approaches to Virulence in C. albicans and C. glabrata: Two Sides of the Same Coin

2019 ◽  
Vol 20 (9) ◽  
pp. 2345 ◽  
Author(s):  
Mónica Galocha ◽  
Pedro Pais ◽  
Mafalda Cavalheiro ◽  
Diana Pereira ◽  
Romeu Viana ◽  
...  
Keyword(s):  
Stress Resistance ◽  
Biofilm Formation ◽  
Candida Glabrata ◽  
Resistance Mechanisms ◽  
Dependent Manner ◽  
Fungal Virulence ◽  
Tissue Invasion ◽  
Etiologic Agents ◽  
Two Sides ◽  
Secreted Enzymes

Candida albicans and Candida glabrata are the two most prevalent etiologic agents of candidiasis worldwide. Although both are recognized as pathogenic, their choice of virulence traits is highly divergent. Indeed, it appears that these different approaches to fungal virulence may be equally successful in causing human candidiasis. In this review, the virulence mechanisms employed by C. albicans and C. glabrata are analyzed, with emphasis on the differences between the two systems. Pathogenesis features considered in this paper include dimorphic growth, secreted enzymes and signaling molecules, and stress resistance mechanisms. The consequences of these traits in tissue invasion, biofilm formation, immune system evasion, and macrophage escape, in a species dependent manner, are discussed. This review highlights the observation that C. albicans and C. glabrata follow different paths leading to a similar outcome. It also highlights the lack of knowledge on some of the specific mechanisms underlying C. glabrata pathogenesis, which deserve future scrutiny.

scholarly journals Relative Abundances ofCandida albicansandCandida glabratainIn VitroCoculture Biofilms Impact Biofilm Structure and Formation

2018 ◽  
Vol 84 (8) ◽  
pp. e02769-17 ◽  
Author(s):  
Michelle L. Olson ◽  
Arul Jayaraman ◽  
Katy C. Kao
Keyword(s):  
Gene Expression ◽  
Candida Albicans ◽  
Biofilm Formation ◽  
Candida Glabrata ◽  
Interspecific Interactions ◽  
Host Immune System ◽  
Dependent Manner ◽  
Important Species ◽  
Content Type ◽  
Content Ratio

ABSTRACTCandidais a member of the normal human microbiota and often resides on mucosal surfaces such as the oral cavity or the gastrointestinal tract. In addition to their commensality,Candidaspecies can opportunistically become pathogenic if the host microbiota is disrupted or if the host immune system becomes compromised. An important factor forCandidapathogenesis is its ability to form biofilm communities. The two most medically important species—Candida albicansandCandida glabrata—are often coisolated from infection sites, suggesting the importance ofCandidacoculture biofilms. In this work, we report that biofilm formation of the coculture population depends on the relative ratio of starting cell concentrations ofC. albicansandC. glabrata. When using a starting ratio ofC. albicanstoC. glabrataof 1:3, ∼6.5- and ∼2.5-fold increases in biofilm biomass were observed relative to those of aC. albicansmonoculture and aC. albicans/C. glabrataratio of 1:1, respectively. Confocal microscopy analysis revealed the heterogeneity and complex structures composed of longC. albicanshyphae andC. glabratacell clusters in the coculture biofilms, and reverse transcription-quantitative PCR (qRT-PCR) studies showed increases in the relative expression of theHWP1andALS3adhesion genes in theC. albicans/C. glabrata1:3 biofilm compared to that in theC. albicansmonoculture biofilm. Additionally, only the 1:3C. albicans/C. glabratabiofilm demonstrated an increased resistance to the antifungal drug caspofungin. Overall, the results suggest that interspecific interactions between these two fungal pathogens increase biofilm formation and virulence-related gene expression in a coculture composition-dependent manner.IMPORTANCECandida albicansandCandida glabrataare often coisolated during infection, and the occurrence of coisolation increases with increasing inflammation, suggesting possible synergistic interactions between the twoCandidaspecies in pathogenesis. During the course of an infection, the prevalence of eachCandidaspecies may change over time due to differences in metabolism and in the resistance of each species to antifungal therapies. Therefore, it is necessary to understand the dynamics betweenC. albicansandC. glabratain coculture to develop better therapeutic strategies againstCandidainfections. Existingin vitrowork has focused on understanding how an equal-part culture ofC. albicansandC. glabrataimpacts biofilm formation and pathogenesis. What is not understood, and what is investigated in this work, is how the composition ofCandidaspecies in coculture impacts overall biofilm formation, virulence gene expression, and the therapeutic treatment of biofilms.

scholarly journals Natural and Enantiopure Alkylglycerols as Antibiofilms Against Clinical Bacterial Isolates and Quorum Sensing Inhibitors of Chromobacterium violaceum ATCC 12472

Antibiotics ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 430
Author(s):  
Klauss E. Chaverra Daza ◽  
Edelberto Silva Gómez ◽  
Bárbara D. Moreno Murillo ◽  
Humberto Mayorga Wandurraga
Keyword(s):  
Quorum Sensing ◽  
Biofilm Formation ◽  
Microtiter Plate ◽  
Resistance Mechanisms ◽  
Chromobacterium Violaceum ◽  
Dependent Manner ◽  
Bacterial Isolates ◽  
Concentration Dependent Manner ◽  
Biofilm Inhibition ◽  
Microtiter Plate Assay

Resistance mechanisms occur in almost all clinical bacterial isolates and represent one of the most worrisome health problems worldwide. Bacteria can form biofilms and communicate through quorum sensing (QS), which allow them to develop resistance against conventional antibiotics. Thus, new therapeutic candidates are sought. We focus on alkylglycerols (AKGs) because of their recently discovered quorum sensing inhibition (QSI) ability and antibiofilm potential. Fifteen natural enantiopure AKGs were tested to determine their effect on the biofilm formation of other clinical bacterial isolates, two reference strains and their QSI was determined using Chromobacterium violaceum ATCC 12472. The highest biofilm inhibition rates (%) and minimum QS inhibitory concentration were determined by a microtiter plate assay and ciprofloxacin was used as the standard antibiotic. At subinhibitory concentrations, each AKG reduced biofilm formation in a concentration-dependent manner against seven bacterial isolates, with values up to 97.2%. Each AKG displayed QSI at different levels of ability without affecting the growth of C. violaceum. AKG (2S)-3-O-(cis-13’-docosenyl)-1,2-propanediol was the best QS inhibitor (20 μM), while (2S)-3-O-(cis-9’-hexadecenyl)-1,2-propanediol was the least effective (795 μM). The results showed for the first time the QSI activity of this natural AKG series and suggest that AKGs could be promising candidates for further studies on preventing antimicrobial resistance.

Antibiotics Application Strategies to Control Biofilm Formation in Pathogenic Bacteria

2020 ◽  
Vol 21 (4) ◽  
pp. 270-286 ◽  
Author(s):  
Fazlurrahman Khan ◽  
Dung T.N. Pham ◽  
Sandra F. Oloketuyi ◽  
Young-Mog Kim
Keyword(s):  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Extracellular Polymeric Substances ◽  
Quorum Quenching ◽  
Resistance Mechanisms ◽  
Bacterial Biofilm ◽  
Bacterial Cells ◽  
High Concentration ◽  
Biofilm Inhibition ◽  
Abiotic Surfaces

Background: The establishment of a biofilm by most pathogenic bacteria has been known as one of the resistance mechanisms against antibiotics. A biofilm is a structural component where the bacterial community adheres to the biotic or abiotic surfaces by the help of Extracellular Polymeric Substances (EPS) produced by bacterial cells. The biofilm matrix possesses the ability to resist several adverse environmental factors, including the effect of antibiotics. Therefore, the resistance of bacterial biofilm-forming cells could be increased up to 1000 times than the planktonic cells, hence requiring a significantly high concentration of antibiotics for treatment. Methods: Up to the present, several methodologies employing antibiotics as an anti-biofilm, antivirulence or quorum quenching agent have been developed for biofilm inhibition and eradication of a pre-formed mature biofilm. Results: Among the anti-biofilm strategies being tested, the sub-minimal inhibitory concentration of several antibiotics either alone or in combination has been shown to inhibit biofilm formation and down-regulate the production of virulence factors. The combinatorial strategies include (1) combination of multiple antibiotics, (2) combination of antibiotics with non-antibiotic agents and (3) loading of antibiotics onto a carrier. Conclusion: The present review paper describes the role of several antibiotics as biofilm inhibitors and also the alternative strategies adopted for applications in eradicating and inhibiting the formation of biofilm by pathogenic bacteria.

scholarly journals In VitroAnalyses of the Effects of Heparin and Parabens on Candida albicans Biofilms and Planktonic Cells

2011 ◽  
Vol 56 (1) ◽  
pp. 148-153 ◽  
Author(s):  
Marisa H. Miceli ◽  
Stella M. Bernardo ◽  
T. S. Neil Ku ◽  
Carla Walraven ◽  
Samuel A. Lee
Keyword(s):  
Candida Albicans ◽  
Metabolic Activity ◽  
Biofilm Formation ◽  
High Dose ◽  
Dependent Manner ◽  
Planktonic Cells ◽  
Content Type ◽  
Heparin Sodium ◽  
The Individual

ABSTRACTInfections and thromboses are the most common complications associated with central venous catheters. Suggested strategies for prevention and management of these complications include the use of heparin-coated catheters, heparin locks, and antimicrobial lock therapy. However, the effects of heparin onCandida albicansbiofilms and planktonic cells have not been previously studied. Therefore, we sought to determine thein vitroeffect of a heparin sodium preparation (HP) on biofilms and planktonic cells ofC. albicans. Because HP contains two preservatives, methyl paraben (MP) and propyl paraben (PP), these compounds and heparin sodium without preservatives (Pure-H) were also tested individually. The metabolic activity of the mature biofilm after treatment was assessed using XTT [2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide] reduction and microscopy. Pure-H, MP, and PP caused up to 75, 85, and 60% reductions of metabolic activity of the mature preformedC. albicansbiofilms, respectively. Maximal efficacy against the mature biofilm was observed with HP (up to 90%) compared to the individual compounds (P< 0.0001). Pure-H, MP, and PP each inhibitedC. albicansbiofilm formation up to 90%. A complete inhibition of biofilm formation was observed with HP at 5,000 U/ml and higher. When tested against planktonic cells, each compound inhibited growth in a dose-dependent manner. These data indicated that HP, MP, PP, and Pure-H havein vitroantifungal activity againstC. albicansmature biofilms, formation of biofilms, and planktonic cells. Investigation of high-dose heparin-based strategies (e.g., heparin locks) in combination with traditional antifungal agents for the treatment and/or prevention ofC. albicansbiofilms is warranted.

scholarly journals Biofilm inhibition and bactericidal activity of NiTi alloy coated with graphene oxide/silver nanoparticles via electrophoretic deposition

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sirapat Pipattanachat ◽  
Jiaqian Qin ◽  
Dinesh Rokaya ◽  
Panida Thanyasrisung ◽  
Viritpon Srimaneepong
Keyword(s):  
Surface Roughness ◽  
Silver Nanoparticles ◽  
Graphene Oxide ◽  
Electrophoretic Deposition ◽  
Biofilm Formation ◽  
Niti Alloy ◽  
Surface Characteristics ◽  
Dependent Manner ◽  
Biofilm Inhibition ◽  
Coating Time

AbstractBiofilm formation on medical devices can induce complications. Graphene oxide/silver nanoparticles (GO/AgNPs) coated nickel-titanium (NiTi) alloy has been successfully produced. Therefore, the aim of this study was to determine the anti-bacterial and anti-biofilm effects of a GO/AgNPs coated NiTi alloy prepared by Electrophoretic deposition (EPD). GO/AgNPs were coated on NiTi alloy using various coating times. The surface characteristics of the coated NiTi alloy substrates were investigated and its anti-biofilm and anti-bacterial effect on Streptococcus mutans biofilm were determined by measuring the biofilm mass and the number of viable cells using a crystal violet assay and colony counting assay, respectively. The results showed that although the surface roughness increased in a coating time-dependent manner, there was no positive correlation between the surface roughness and the total biofilm mass. However, increased GO/AgNPs deposition produced by the increased coating time significantly reduced the number of viable bacteria in the biofilm (p < 0.05). Therefore, the GO/AgNPs on NiTi alloy have an antibacterial effect on the S. mutans biofilm. However, the increased surface roughness does not influence total biofilm mass formation (p = 0.993). Modifying the NiTi alloy surface using GO/AgNPs can be a promising coating to reduce the consequences of biofilm formation.

scholarly journals Eap1p, an Adhesin That Mediates Candida albicans Biofilm Formation In Vitro and In Vivo

2007 ◽  
Vol 6 (6) ◽  
pp. 931-939 ◽  
Author(s):  
Fang Li ◽  
Michael J. Svarovsky ◽  
Amy J. Karlsson ◽  
Joel P. Wagner ◽  
Karen Marchillo ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Cell Adhesion ◽  
Biofilm Formation ◽  
Fungal Infections ◽  
Gene Dosage ◽  
Venous Catheter ◽  
Flow Chamber ◽  
Dependent Manner

ABSTRACT Candida albicans is the leading cause of systemic fungal infections in immunocompromised humans. The ability to form biofilms on surfaces in the host or on implanted medical devices enhances C. albicans virulence, leading to antimicrobial resistance and providing a reservoir for infection. Biofilm formation is a complex multicellular process consisting of cell adhesion, cell growth, morphogenic switching between yeast form and filamentous states, and quorum sensing. Here we describe the role of the C. albicans EAP1 gene, which encodes a glycosylphosphatidylinositol-anchored, glucan-cross-linked cell wall protein, in adhesion and biofilm formation in vitro and in vivo. Deleting EAP1 reduced cell adhesion to polystyrene and epithelial cells in a gene dosage-dependent manner. Furthermore, EAP1 expression was required for C. albicans biofilm formation in an in vitro parallel plate flow chamber model and in an in vivo rat central venous catheter model. EAP1 expression was upregulated in biofilm-associated cells in vitro and in vivo. Our results illustrate an association between Eap1p-mediated adhesion and biofilm formation in vitro and in vivo.

scholarly journals Bioactive constituents with antibacterial, resistance modulation, anti-biofilm formation and efflux pump inhibition properties from Aidia genipiflora stem bark

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Daniel Anokwah ◽  
Evelyn Asante-Kwatia ◽  
Abraham Y. Mensah ◽  
Cynthia Amaning Danquah ◽  
Benjamin K. Harley ◽  
...  
Keyword(s):  
Biofilm Formation ◽  
Efflux Pump ◽  
Ethyl Acetate Fraction ◽  
Stem Bark ◽  
Resistance Mechanisms ◽  
Bioactive Constituents ◽  
Biofilm Inhibition ◽  
E Coli ◽  
Efflux Pump Inhibition ◽  
Oleanonic Acid

Abstract Background Antimicrobial resistance is a global health challenge. The involvement of bacterial biofilms and efflux pumps in the development of multidrug resistance (MDR) is well established. Medicinal plants have been proposed as alternatives for combating MDR focusing on their bioactive constituents with resistance modulatory activities. This study was aimed at investigating the stem bark of Aidia genipiflora for bioactive constituents with anti-biofilm, efflux pump inhibition and resistance modulatory activities. Method The crude methanol extract was purified by column chromatography and isolated compounds characterized by mass and nuclear magnetic resonance spectrometry. Antibacterial activity was determined by the High-throughput spot culture growth inhibition and the broth micro-dilution assay. The ethidium bromide accumulation assay was used to determine efflux pump inhibition property. Biofilm inhibition was determined in a microplate crystal violet retention assay. Results Purification of the ethyl acetate fraction led to the isolation of oleanonic acid (1), 4-hydroxy cinnamic acid docosyl ester (2), β-stigmasterol/β-sitosterol (mixture 3a/b) and D-mannitol (4). The minimum inhibitory concentrations (MICs) ranged from 250 to > 500 μg/mL for extracts and fractions and from 15 to 250 μg/mL for compounds. In the presence of sub-inhibitory concentrations of the compounds, the MIC of amoxicillin against E. coli (20 μg/mL) and P. aeruginosa (320 μg/mL) was reduced by 32 and 10 folds respectively. The whole extract demonstrated anti-biofilm formation and efflux pump inhibition in E. coli, S. aureus and P. aeruginosa. The sterol mixture (3a/b) at concentration of 100 μg/mL caused the highest inhibition (73%) of biofilm formation in S. aureus. Oleanonic acid (1) demonstrated remarkable efflux pump inhibition at MIC of 7.8 μg/mL in E. coli better than the standard drugs verapamil and chlorpromazine. Conclusion This study confirms the prospects of A. genipiflora as a source of new antibacterial agents and adjuvants that could interact with some resistance mechanisms in bacteria to enhance the activity of hitherto ineffective antibiotics. “A small portion of the study has been presented in a conference in the form of poster”.

scholarly journals Oligoribonuclease is the primary degradative enzyme for pGpG inPseudomonas aeruginosathat is required for cyclic-di-GMP turnover

2015 ◽  
Vol 112 (36) ◽  
pp. E5048-E5057 ◽  
Author(s):  
Mona W. Orr ◽  
Gregory P. Donaldson ◽  
Geoffrey B. Severin ◽  
Jingxin Wang ◽  
Herman O. Sintim ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Active Site ◽  
Half Life ◽  
Biofilm Formation ◽  
Degradation Pathway ◽  
Dependent Manner ◽  
Capillary Action ◽  
Diguanylate Cyclases ◽  
Active Site Mutants ◽  
Degradative Enzyme

The bacterial second messenger cyclic di-GMP (c-di-GMP) controls biofilm formation and other phenotypes relevant to pathogenesis. Cyclic-di-GMP is synthesized by diguanylate cyclases (DGCs). Phosphodiesterases (PDE-As) end signaling by linearizing c-di-GMP to 5ʹ-phosphoguanylyl-(3ʹ,5ʹ)-guanosine (pGpG), which is then hydrolyzed to two GMP molecules by yet unidentified enzymes termed PDE-Bs. We show that pGpG inhibits a PDE-A fromPseudomonas aeruginosa. In a dual DGC and PDE-A reaction, excess pGpG extends the half-life of c-di-GMP, indicating that removal of pGpG is critical for c-di-GMP homeostasis. Thus, we sought to identify the PDE-B enzyme(s) responsible for pGpG degradation. A differential radial capillary action of ligand assay-based screen for pGpG binding proteins identified oligoribonuclease (Orn), an exoribonuclease that hydrolyzes two- to five-nucleotide-long RNAs. Purified Orn rapidly converts pGpG into GMP. To determine whether Orn is the primary enzyme responsible for degrading pGpG, we assayed cell lysates of WT and ∆ornstrains ofP. aeruginosaPA14 for pGpG stability. The lysates from ∆ornshowed 25-fold decrease in pGpG hydrolysis. Complementation with WT, but not active site mutants, restored hydrolysis. Accumulation of pGpG in the ∆ornstrain could inhibit PDE-As, increasing c-di-GMP concentration. In support, we observed increased transcription from the c-di-GMP–regulatedpelpromoter. Additionally, the c-di-GMP–governed auto-aggregation and biofilm phenotypes were elevated in the ∆ornstrain in apel-dependent manner. Finally, we directly detect elevated pGpG and c-di-GMP in the ∆ornstrain. Thus, we identified that Orn serves as the primary PDE-B enzyme that removes pGpG, which is necessary to complete the final step in the c-di-GMP degradation pathway.

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