scholarly journals Effect of Tannic Acid on the Transcriptome of the Soil Bacterium Pseudomonas protegens Pf-5

2013 ◽  
Vol 79 (9) ◽  
pp. 3141-3145 ◽  
Author(s):  
Chee Kent Lim ◽  
Anahit Penesyan ◽  
Karl A. Hassan ◽  
Joyce E. Loper ◽  
Ian T. Paulsen
Keyword(s):  
Tannic Acid ◽  
Biofilm Formation ◽  
Sulfur Metabolism ◽  
Antimicrobial Properties ◽  
Hydrolysable Tannin ◽  
Content Type ◽  
Metal Chelating ◽  
Expression Of Genes ◽  
Secondary Metabolite Biosynthesis ◽  
Iron And Zinc

ABSTRACTTannins are a diverse group of plant-produced, polyphenolic compounds with metal-chelating and antimicrobial properties that are prevalent in many soils. Using transcriptomics, we determined that tannic acid, a form of hydrolysable tannin, broadly affects the expression of genes involved in iron and zinc homeostases, sulfur metabolism, biofilm formation, motility, and secondary metabolite biosynthesis in the soil- and rhizosphere-inhabiting bacteriumPseudomonas protegensPf-5.

scholarly journals Loss of Function inEscherichia coliExposed to Environmentally Relevant Concentrations of Benzalkonium Chloride

2018 ◽  
Vol 85 (4) ◽  
Author(s):  
Sarah Forbes ◽  
Nicola Morgan ◽  
Gavin J. Humphreys ◽  
Alejandro Amézquita ◽  
Hitesh Mistry ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Growth Rate ◽  
Biofilm Formation ◽  
Benzalkonium Chloride ◽  
Loss Of Function ◽  
Free Medium ◽  
Content Type ◽  
Expression Of Genes ◽  
Repeated Passage

ABSTRACTAssessing the risk of resistance associated with biocide exposure commonly involves exposing microorganisms to biocides at concentrations close to the MIC. With the aim of representing exposure to environmental biocide residues,Escherichia coliMG1655 was grown for 20 passages in the presence or absence of benzalkonium chloride (BAC) at 100 ng/liter and 1,000 ng/liter (0.0002% and 0.002% of the MIC, respectively). BAC susceptibility, planktonic growth rates, motility, and biofilm formation were assessed, and differentially expressed genes were determined via transcriptome sequencing. Planktonic growth rate and biofilm formation were significantly reduced (P< 0.001) following BAC adaptation, while BAC minimum bactericidal concentration increased 2-fold. Transcriptomic analysis identified 289 upregulated and 391 downregulated genes after long-term BAC adaptation compared with the respective control organism passaged in BAC-free medium. When the BAC-adapted bacterium was grown in BAC-free medium, 1,052 genes were upregulated and 753 were downregulated. Repeated passage solely in biocide-free medium resulted in 460 upregulated and 476 downregulated genes compared with unexposed bacteria. Long-term exposure to environmentally relevant BAC concentrations increased the expression of genes associated with efflux and reduced the expression of genes associated with outer-membrane porins, motility, and chemotaxis. This was manifested phenotypically through the loss of function (motility). Repeated passage in a BAC-free environment resulted in the upregulation of multiple respiration-associated genes, which was reflected by increased growth rate. In summary, repeated exposure ofE. colito BAC residues resulted in significant alterations in global gene expression that were associated with minor decreases in biocide susceptibility, reductions in growth rate and biofilm formation, and loss of motility.IMPORTANCEExposure to very low concentrations of biocides in the environment is a poorly understood risk factor for antimicrobial resistance. Repeated exposure to trace levels of the biocide benzalkonium chloride (BAC) resulted in loss of function (motility) and a general reduction in bacterial fitness but relatively minor decreases in susceptibility. These changes were accompanied by widespread changes in theEscherichia colitranscriptome. These results demonstrate the importance of including phenotypic characterization in studies designed to assess the risks of biocide exposure.

scholarly journals Genome-Wide Transcription Profiling of the Early Phase of Biofilm Formation by Candida albicans

2005 ◽  
Vol 4 (9) ◽  
pp. 1562-1573 ◽  
Author(s):  
Luis A. Murillo ◽  
George Newport ◽  
Chung-Yu Lan ◽  
Stefan Habelitz ◽  
Jan Dungan ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Biofilm Formation ◽  
Early Stage ◽  
Sulfur Metabolism ◽  
Single Cells ◽  
Alternative Pathway ◽  
Opportunistic Pathogen ◽  
Abiotic Surfaces ◽  
Expression Of Genes ◽  
Structure Changes

ABSTRACT The ability to adhere to surfaces and develop as a multicellular community is an adaptation used by most microorganisms to survive in changing environments. Biofilm formation proceeds through distinct developmental phases and impacts not only medicine but also industry and evolution. In organisms such as the opportunistic pathogen Candida albicans, the ability to grow as biofilms is also an important mechanism for persistence, facilitating its growth on different tissues and a broad range of abiotic surfaces used in medical devices. The early stage of C. albicans biofilm is characterized by the adhesion of single cells to the substratum, followed by the formation of an intricate network of hyphae and the beginning of a dense structure. Changes in the transcriptome begin within 30 min of contact with the substrate and include expression of genes related to sulfur metabolism, in particular MET3, and the equivalent gene homologues of the Ribi regulon in Saccharomyces cerevisiae. Some of these changes are initiated early and maintained throughout the process; others are restricted to the earliest stages of biofilm formation. We identify here a potential alternative pathway for cysteine metabolism and the biofilm-associated expression of genes involved in glutathione production in C. albicans.

scholarly journals The Transcriptional Regulator BpsR Controls the Growth ofBordetella bronchisepticaby Repressing Genes Involved in Nicotinic Acid Degradation

2018 ◽  
Vol 200 (12) ◽  
pp. e00712-17 ◽  
Author(s):  
Manita Guragain ◽  
Jamie Jennings-Gee ◽  
Natalia Cattelan ◽  
Mary Finger ◽  
Matt S. Conover ◽  
...  
Keyword(s):  
Nicotinic Acid ◽  
Biofilm Formation ◽  
Transcriptional Control ◽  
Bordetella Bronchiseptica ◽  
Negative Regulator ◽  
Growth Defect ◽  
Content Type ◽  
Polysaccharide Production ◽  
Expression Of Genes

ABSTRACTMany of the pathogenic species of the genusBordetellahave an absolute requirement for nicotinic acid (NA) for laboratory growth. These Gram-negative bacteria also harbor a gene cluster homologous to theniccluster ofPseudomonas putidawhich is involved in the aerobic degradation of NA and its transcriptional control. We report here that BpsR, a negative regulator of biofilm formation and Bps polysaccharide production, controls the growth ofBordetella bronchisepticaby repressing the expression ofnicgenes. The severe growth defect of the ΔbpsRstrain in Stainer-Scholte medium was restored by supplementation with NA, which also functioned as an inducer ofnicgenes at low micromolar concentrations that are usually present in animals and humans. Purified BpsR protein bound to thenicpromoter region, and its DNA binding activity was inhibited by 6-hydroxynicotinic acid (6-HNA), the first metabolite of the NA degradative pathway. Reporter assays with the isogenic mutant derivative of the wild-type (WT) strain harboring deletion innicA, which encodes a putative nicotinic acid hydroxylase responsible for conversion of NA to 6-HNA, showed that 6-HNA is the actual inducer of thenicgenes in the bacterial cell. Gene expression profiling further showed that BpsR dually activated and repressed the expression of genes associated with pathogenesis, transcriptional regulation, metabolism, and other cellular processes. We discuss the implications of these findings with respect to the selection of pyridines such as NA and quinolinic acid for optimum bacterial growth depending on the ecological niche.IMPORTANCEBpsR, the previously described regulator of biofilm formation and Bps polysaccharide production, controlsBordetella bronchisepticagrowth by regulating the expression of genes involved in the degradation of nicotinic acid (NA). 6-Hydroxynicotinic acid (6-HNA), the first metabolite of the NA degradation pathway prevented BpsR from binding to DNA and was the actualin vivoinducer. We hypothesize that BpsR enablesBordetellabacteria to efficiently and selectively utilize NA for their survival depending on the environment in which they reside. The results reported herein lay the foundation for future investigations of how BpsR and the alteration of its activity by NA orchestrate the control ofBordetellagrowth, metabolism, biofilm formation, and pathogenesis.

scholarly journals Tannic Acid Inhibits Staphylococcus aureus Surface Colonization in an IsaA-Dependent Manner

2012 ◽  
Vol 81 (2) ◽  
pp. 496-504 ◽  
Author(s):  
David E. Payne ◽  
Nicholas R. Martin ◽  
Katherine R. Parzych ◽  
Alex H. Rickard ◽  
Adam Underwood ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Tannic Acid ◽  
Biofilm Formation ◽  
Antibiofilm Activity ◽  
Host Immune System ◽  
Dependent Manner ◽  
Content Type ◽  
Surface Colonization ◽  
Biofilm Development ◽  
Insight Into

ABSTRACTStaphylococcus aureusis a human commensal and pathogen that is capable of forming biofilms on a variety of host tissues and implanted medical devices. Biofilm-associated infections resist antimicrobial chemotherapy and attack from the host immune system, making these infections particularly difficult to treat. In order to gain insight into environmental conditions that influenceS. aureusbiofilm development, we screened a library of small molecules for the ability to inhibitS. aureusbiofilm formation. This led to the finding that the polyphenolic compound tannic acid inhibitsS. aureusbiofilm formation in multiple biofilm models without inhibiting bacterial growth. We present evidence that tannic acid inhibitsS. aureusbiofilm formation via a mechanism dependent upon the putative transglycosylase IsaA. Tannic acid did not inhibit biofilm formation of anisaAmutant. Overexpression of wild-type IsaA inhibited biofilm formation, whereas overexpression of a catalytically dead IsaA had no effect. Tannin-containing drinks like tea have been found to reduce methicillin-resistantS. aureusnasal colonization. We found that black tea inhibitedS. aureusbiofilm development and that anisaAmutant resisted this inhibition. Antibiofilm activity was eliminated from tea when milk was added to precipitate the tannic acid. Finally, we developed a rodent model forS. aureusthroat colonization and found that tea consumption reducedS. aureusthroat colonization via anisaA-dependent mechanism. These findings provide insight into a molecular mechanism by which commonly consumed polyphenolic compounds, such as tannins, influenceS. aureussurface colonization.

scholarly journals Inhibition of Biofilm Formation by Esomeprazole in Pseudomonas aeruginosa and Staphylococcus aureus

2012 ◽  
Vol 56 (8) ◽  
pp. 4360-4364 ◽  
Author(s):  
Vandana Singh ◽  
Vaneet Arora ◽  
M. Jahangir Alam ◽  
Kevin W. Garey
Keyword(s):  
Staphylococcus Aureus ◽  
Pseudomonas Aeruginosa ◽  
Bacterial Growth ◽  
Biofilm Formation ◽  
Antimicrobial Properties ◽  
Antibiofilm Activity ◽  
Biofilm Growth ◽  
Content Type ◽  
Conventional Antibiotics ◽  
And Staphylococcus Aureus

ABSTRACTStaphylococcus aureusandPseudomonas aeruginosaare common nosocomial pathogens responsible for biofilm-associated infections. Proton pump inhibitors (PPI), such as esomeprazole, may have novel antimicrobial properties. The objective of this study was to assess whether esomeprazole prevents sessile bacterial growth and biofilm formation and whether it may have synergistic killing effects with standard antibiotics. The antibiofilm activity of esomeprazole at 0.25 mM was tested against two strains each ofS. aureusandP. aeruginosa. Bacterial biofilms were prepared using a commercially available 96-peg-plate Calgary biofilm device. Sessile bacterial CFU counts and biomass were assessed during 72 hours of esomeprazole exposure. The killing activities after an additional 24 hours of vancomycin (againstS. aureus) and meropenem (againstP. aeruginosa) treatment with or without preexposure to esomeprazole were also assessed by CFU and biomass analyses.P. aeruginosaandS. aureusstrains exposed to esomeprazole displayed decreased sessile bacterial growth and biomass (P< 0.001, each parameter). After 72 h of exposure, there was a 1-log10decrease in the CFU/ml of esomeprazole-exposedP. aeruginosaandS. aureusstrains compared to controls (P< 0.001). After 72 h of exposure, measured absorbance was 100% greater inP. aeruginosacontrol strains than in esomeprazole-exposed strains (P< 0.001). Increased killing and decreased biomass were observed for esomeprazole-treated bacteria compared to untreated controls exposed to conventional antibiotics (P< 0.001, each parameter). Reduced biofilm growth after 24 h was visibly apparent by light micrographs forP. aeruginosaandS. aureusisolates exposed to esomeprazole compared to untreated controls. In conclusion, esomeprazole demonstrated an antibiofilm effect against biofilm-producingS. aureusandP. aeruginosa.

scholarly journals Regulation ofwaaHby PhoB during PiStarvation Promotes Biofilm Formation byEscherichia coliO157:H7

2019 ◽  
Vol 201 (18) ◽  
Author(s):  
Philippe Vogeleer ◽  
Antony T. Vincent ◽  
Samuel M. Chekabab ◽  
Steve J. Charette ◽  
Alexey Novikov ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Biofilm Formation ◽  
Ecological Niches ◽  
Pho Regulon ◽  
Starvation Stress ◽  
Content Type ◽  
E Coli ◽  
Expression Of Genes ◽  
K 12 ◽  
Pst System

ABSTRACTIn open environments such as water, enterohemorrhagicEscherichia coliO157:H7 responds to inorganic phosphate (Pi) starvation by inducing the Pho regulon controlled by PhoB. This activates the phosphate-specific transport (Pst) system that contains a high-affinity Pitransporter. In the Δpstmutant, PhoB is constitutively activated and regulates the expression of genes in the Pho regulon. Here, we show that Pistarvation and deletion of thepstsystem enhanceE. coliO157:H7 biofilm formation. Among differentially expressed genes of EDL933 grown under Pistarvation conditions and in the Δpstmutant, we have found that a member of the PhoB regulon,waaH, predicted to encode a glycosyltransferase, was highly expressed. Interestingly, WaaH contributed to biofilm formation ofE. coliO157:H7 during both Pistarvation and in the Δpstmutant. In the Δpstmutant, the presence ofwaaHwas associated with lipopolysaccharide (LPS) R3 core type modifications, whereas inE. coliO157:H7,waaHoverexpression had no effect on LPS structure during Pistarvation. Therefore,waaHparticipates inE. coliO157:H7 biofilm formation during Pistarvation, but its biochemical role remains to be clarified. This study highlights the importance of the Pistarvation stress response to biofilm formation, which may contribute to the persistence ofE. coliO157:H7 in the environment.IMPORTANCEEnterohemorrhagicEscherichia coliO157:H7 is a human pathogen that causes bloody diarrhea that can result in renal failure. Outside of mammalian hosts,E. coliO157:H7 survives for extended periods of time in nutrient-poor environments, likely as part of biofilms. InE. coliK-12, the levels of free extracellular Piaffect biofilm formation; however, it was unknown whether Piinfluences biofilm formation byE. coliO157:H7. Our results show that upon Pistarvation, PhoB activateswaaHexpression, which favors biofilm formation byE. coliO157:H7. These findings suggest that WaaH is a target for controlling biofilm formation. Altogether, our work demonstrates how adaptation to Pistarvation allowsE. coliO157:H7 to occupy different ecological niches.

scholarly journals Glucose-6-Phosphate Acts as an Extracellular Signal of SagS To Modulate Pseudomonas aeruginosa c-di-GMP Levels, Attachment, and Biofilm Formation

mSphere ◽  
2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Soyoung Park ◽  
Jozef Dingemans ◽  
Madison Gowett ◽  
Karin Sauer
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Biofilm Formation ◽  
Opportunistic Pathogen ◽  
Marker Genes ◽  
Dependent Manner ◽  
Content Type ◽  
Expression Of Genes ◽  
Extracellular Signal ◽  
Two Component ◽  
Sense And Respond

ABSTRACT In Pseudomonas aeruginosa, the orphan two-component sensor SagS contributes both to transition to biofilm formation and to biofilm cells gaining their heightened tolerance to antimicrobials. However, little is known about the identity of the signals or conditions sensed by SagS to induce the switch to the sessile, drug-tolerant mode of growth. Using a modified Biolog phenotype assay to screen for compounds that modulate attachment in a SagS-dependent manner, we identified glucose-6-phosphate to enhance attachment in a manner dependent on the glucose-6-phosphate concentration and SagS. The stimulatory effect was not limited to the attachment since glucose-6-phosphate likewise enhanced biofilm formation and also enhanced the expression of select biofilm marker genes. Moreover, exposure to glucose-6-phosphate coincided with decreased swarming motility but increased cellular cyclic-di-GMP (c-di-GMP) levels in biofilms. No such response was noted for compounds modulating attachment and biofilm formation in a manner independent of SagS. Modulation of c-di-GMP in response to glucose-6-phosphate was due to the diguanylate cyclase NicD, with NicD also being required for enhanced biofilm formation. The latter was independent of the sensory domain of NicD but dependent on NicD activity, SagS, and the interaction between NicD and SagS. Our findings indicate that glucose-6-phosphate likely mimics a signal or conditions sensed by SagS to activate its motile-sessile switch function. In addition, our findings provide new insight into the interfaces between the ligand-mediated two-component system signaling pathway and c-di-GMP levels. IMPORTANCE Pathogens sense and respond to signals and cues present in their environment, including host-derived small molecules to modulate the expression of their virulence repertoire. Here, we demonstrate that the opportunistic pathogen Pseudomonas aeruginosa responds to glucose-6-phosphate. Since glucose-6-phosphate is primarily made available due to cell lysis, it is likely that glucose-6-phosphate represents a cross-kingdom cell-to-cell signal that enables P. aeruginosa to adapt to the (nutrient-poor) host environment by enhancing biofilm formation, cyclic-di-GMP, and the expression of genes linked to biofilm formation in a concentration- and SagS-dependent manner.

scholarly journals TosR-Mediated Regulation of Adhesins and Biofilm Formation in UropathogenicEscherichia coli

mSphere ◽  
2018 ◽  
Vol 3 (3) ◽  
Author(s):  
Courtney L. Luterbach ◽  
Valerie S. Forsyth ◽  
Michael D. Engstrom ◽  
Harry L. T. Mobley
Keyword(s):  
Urinary Tract ◽  
Cross Talk ◽  
Biofilm Formation ◽  
Dependent Manner ◽  
Rna Seq ◽  
Concentration Dependent Manner ◽  
Content Type ◽  
E Coli ◽  
Expression Of Genes ◽  
Invasive Infections

ABSTRACTUropathogenicEscherichia colistrains utilize a variety of adherence factors that assist in colonization of the host urinary tract. TosA (typeonesecretionA) is a nonfimbrial adhesin that is predominately expressed during murine urinary tract infection (UTI), binds to kidney epithelial cells, and promotes survival during invasive infections. ThetosRCBDAEFoperon encodes the secretory machinery necessary for TosA localization to theE. colicell surface, as well as the transcriptional regulator TosR. TosR binds upstream of thetosoperon and in a concentration-dependent manner either induces or repressestosAexpression. TosR is a member of the PapB family of fimbrial regulators that can participate in cross talk between fimbrial operons. TosR also binds upstream of thepapoperon and suppresses PapA production. However, the scope of TosR-mediated cross talk is understudied and may be underestimated. To quantify the global effects of TosR-mediated regulation on theE. coliCFT073 genome, we induced expression oftosR, collected mRNA, and performed high-throughput RNA sequencing (RNA-Seq). These findings show that production of TosR affected the expression of genes involved with adhesins, including P, F1C, and Auf fimbriae, nitrate-nitrite transport, microcin secretion, and biofilm formation.IMPORTANCEUropathogenicE. colistrains cause the majority of UTIs, which are the second most common bacterial infection in humans. During a UTI, bacteria adhere to cells within the urinary tract, using a number of different fimbrial and nonfimbrial adhesins. Biofilms can also develop on the surfaces of catheters, resulting in complications such as blockage. In this work, we further characterized the regulator TosR, which links both adhesin production and biofilm formation and likely plays a crucial function during UTI and disseminated infection.

scholarly journals The Candida albicans TOR-Activating GTPases Gtr1 and Rhb1 Coregulate Starvation Responses and Biofilm Formation

mSphere ◽  
2017 ◽  
Vol 2 (6) ◽  
Author(s):  
Peter R. Flanagan ◽  
Ning-Ning Liu ◽  
Darren J. Fitzpatrick ◽  
Karsten Hokamp ◽  
Julia R. Köhler ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Fungal Pathogen ◽  
Biofilm Formation ◽  
Nitrogen Starvation ◽  
Antifungal Drugs ◽  
Target Of Rapamycin ◽  
Content Type ◽  
Expression Of Genes ◽  
Wide Range

ABSTRACT Candida albicans is the major fungal pathogen of humans and is responsible for a wide range of infections, including life-threatening systemic infections in susceptible hosts. Target of rapamycin complex 1 (TORC1) is an essential regulator of metabolism in this fungus, and components of this complex are under increased investigation as targets for new antifungal drugs. The present study characterized the role of GTR1, encoding a putative GTPase, in TORC1 activation. This study shows that GTR1 encodes a protein required for activation of TORC1 activity in response to amino acids and regulation of nitrogen starvation responses. GTR1 mutants show increased cell-cell adhesion and biofilm formation and increased expression of genes involved in these processes. This study demonstrates that starvation responses and biofilm formation are coregulated by GTR1 and suggests that these responses are linked to compete with the microbiome for space and nutrients. Target of rapamycin complex 1 (TORC1) is an essential regulator of metabolism in eukaryotic cells and in the fungal pathogen Candida albicans regulates morphogenesis and nitrogen acquisition. Gtr1 encodes a highly conserved GTPase that in Saccharomyces cerevisiae regulates nitrogen sensing and TORC1 activation. Here, we characterize the role of C. albicans GTR1 in TORC1 activation and compare it with the previously characterized GTPase Rhb1. A homozygous gtr1/gtr1 mutant exhibited impaired TORC1-mediated phosphorylation of ribosomal protein S6 and increased susceptibility to rapamycin. Overexpression of GTR1 impaired nitrogen starvation-induced filamentous growth, MEP2 expression, and growth in bovine serum albumin as the sole nitrogen source. Both GTR1 and RHB1 were shown to regulate genes involved in ribosome biogenesis, amino acid biosynthesis, and expression of biofilm growth-induced genes. The rhb1/rhb1 mutant exhibited a different pattern of expression of Sko1-regulated genes and increased susceptibility to Congo red and calcofluor white. The homozygous gtr1/gtr1 mutant exhibited enhanced flocculation phenotypes and, similar to the rhb1/rhb1 mutant, exhibited enhanced biofilm formation on plastic surfaces. In summary, Gtr1 and Rhb1 link nutrient sensing and biofilm formation and this connectivity may have evolved to enhance the competitiveness of C. albicans in niches where there is intense competition with other microbes for space and nutrients. IMPORTANCE Candida albicans is the major fungal pathogen of humans and is responsible for a wide range of infections, including life-threatening systemic infections in susceptible hosts. Target of rapamycin complex 1 (TORC1) is an essential regulator of metabolism in this fungus, and components of this complex are under increased investigation as targets for new antifungal drugs. The present study characterized the role of GTR1, encoding a putative GTPase, in TORC1 activation. This study shows that GTR1 encodes a protein required for activation of TORC1 activity in response to amino acids and regulation of nitrogen starvation responses. GTR1 mutants show increased cell-cell adhesion and biofilm formation and increased expression of genes involved in these processes. This study demonstrates that starvation responses and biofilm formation are coregulated by GTR1 and suggests that these responses are linked to compete with the microbiome for space and nutrients.

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.

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