scholarly journals Enterococcus faecalis Enhances Candida albicans Mediated Tissue Destruction in a Strain-Dependent Manner

2020 ◽  
Author(s):  
Akshaya Lakshmi Krishnamoorthy ◽  
Alex A Lemus ◽  
Adline Princy Solomon ◽  
Alex M Valm ◽  
Prasanna Neelakantan
Keyword(s):  
Candida Albicans ◽  
Enterococcus Faecalis ◽  
Opportunistic Pathogen ◽  
Clinical Isolates ◽  
Surface Erosion ◽  
Host Immune System ◽  
Dependent Manner ◽  
Tissue Destruction ◽  
Fungal Invasion ◽  
Strain Dependent

Candida albicans as an opportunistic pathogen exploits the host immune system and causes a variety of life-threatening infections. The polymorphic nature of this fungus gives it tremendous advantage to breach mucosal barriers and cause a variety of oral and disseminated infections. Enterococcus faecalis, another opportunistic pathogen co-exists with C. albicans in several niches in the human body, including the oral cavity and gastrointestinal tract. However, interactions between E. faecalis and C. albicans on oral mucosal surfaces remain unknown. Here, for the first time, we comprehensively characterized the interactive profiles between laboratory and clinical isolates of C. albicans (SC5314 and BF1) and E. faecalis (OG1RF and 846) on an organotypic oral mucosal model. Our results demonstrated that the two species formed robust biofilms on the mucosal tissue surface with profound surface erosion and fungal invasion. Specifically, this effect was more pronounced in the laboratory isolates than in the clinical isolates. Notably, several genes of C. albicans involved in tissue adhesion, hyphal formation, fungal invasion, and biofilm formation were significantly upregulated in the presence of E. faecalis. This study highlights the strain-dependent cross-kingdom interactions between E. faecalis and C. albicans on oral mucosa, demonstrating the requisite to study more substrate-dependent polymicrobial interactions.

scholarly journals Interactions between Candida albicans and Enterococcus faecalis in an Organotypic Oral Epithelial Model

2020 ◽  
Vol 8 (11) ◽  
pp. 1771
Author(s):  
Akshaya Lakshmi Krishnamoorthy ◽  
Alex A. Lemus ◽  
Adline Princy Solomon ◽  
Alex M. Valm ◽  
Prasanna Neelakantan
Keyword(s):  
Candida Albicans ◽  
Enterococcus Faecalis ◽  
Biofilm Formation ◽  
Opportunistic Pathogen ◽  
Surface Erosion ◽  
Host Immune System ◽  
Microbial Invasion ◽  
Mucosal Surfaces ◽  
Life Threatening ◽  
Hyphal Formation

Candida albicans as an opportunistic pathogen exploits the host immune system and causes a variety of life-threatening infections. The polymorphic nature of this fungus gives it tremendous advantage to breach mucosal barriers and cause oral and disseminated infections. Similar to C. albicans, Enterococcus faecalis is a major opportunistic pathogen, which is of critical concern in immunocompromised patients. There is increasing evidence that E. faecalis co-exists with C. albicans in the human body in disease samples. While the interactive profiles between these two organisms have been studied on abiotic substrates and mouse models, studies on their interactions on human oral mucosal surfaces are non-existent. Here, for the first time, we comprehensively characterized the interactive profiles between laboratory and clinical isolates of C. albicans (SC5314 and BF1) and E. faecalis (OG1RF and P52S) on an organotypic oral mucosal model. Our results demonstrated that the dual species biofilms resulted in profound surface erosion and significantly increased microbial invasion into mucosal compartments, compared to either species alone. Notably, several genes of C. albicans involved in tissue adhesion, hyphal formation, fungal invasion, and biofilm formation were significantly upregulated in the presence of E. faecalis. By contrast, E. faecalis genes involved in quorum sensing, biofilm formation, virulence, and mammalian cell invasion were downregulated. This study highlights the synergistic cross-kingdom interactions between E. faecalis and C. albicans in mucosal tissue invasion.

scholarly journals Robust, Comprehensive Molecular, and Phenotypical Characterisation of Atypical Candida albicans Clinical Isolates From Bogotá, Colombia

2020 ◽  
Vol 10 ◽  
Author(s):  
Giovanni Rodríguez-Leguizamón ◽  
Andrés Ceballos-Garzón ◽  
Carlos F. Suárez ◽  
Manuel A. Patarroyo ◽  
Claudia M. Parra-Giraldo
Keyword(s):  
Candida Albicans ◽  
Galleria Mellonella ◽  
Opportunistic Pathogen ◽  
Clinical Isolates ◽  
High Genetic Diversity ◽  
Cluster Membership ◽  
Protein Mass ◽  
Molecular Tests ◽  
Well Differentiated ◽  
Clade 1

Candida albicans is commensal in human microbiota and is known to be the commonest opportunistic pathogen, having variable clinical outcomes that can lead to up to 60% mortality. Such wide clinical behaviour can be attributed to its phenotypical plasticity and high genetic diversity. This study characterised 10 Colombian clinical isolates which had already been identified as C. albicans by molecular tests; however, previous bioinformatics analysis of protein mass spectra and phenotypical characteristics has shown that this group of isolates has atypical behaviour, sharing characteristics of both C. africana and C. albicans. This study was aimed at evaluating atypical isolates’ pathogenic capability in the Galleria mellonella model; susceptibility profiles were determined and MLST was used for molecular characterisation. Cluster analysis, enabling unbiased bootstrap to classify the isolates and establish their cluster membership and e-BURST, was used for establishing clonal complexes (CC). Both approaches involved using representative MLST data from the 18 traditional C. albicans clades, as well as C. albicans-associated and minor species. Ten atypical isolates were distributed as follows: 6/10 (B71, B41, B60, R6, R41, and R282) were grouped into a statistically well-supported atypical cluster (AC) and constituted a differentiated CC 6; 2/10 of the isolates were clearly grouped in clade 1 and were concurrent in CC 4 (B80, B44). Another 2/10 atypical isolates were grouped in clade 10 and concurred in CC 7 (R425, R111); most atypical isolates were related to geographically distant isolates and some represented new ST. Isolates B41 and R41 in the AC had greater virulence. Isolate B44 was fluconazole-resistant and was grouped in clade 1. The atypical nature of the isolates studied here was demonstrated by the contrast between phenotypical traits (C. africana-like), molecular markers (C. albicans-like), virulence, and antifungal resistance, highlighting the widely described genetic plasticity for this genus. Our results showed that the atypical isolates forming well-differentiated groups belonged to C. albicans. Our findings could contribute towards developing molecular epidemiology approaches for managing hospital-acquired infection.

scholarly journals Candidalysin Crucially Contributes to Nlrp3 Inflammasome Activation by Candida albicans Hyphae

mBio ◽  
2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Ona Rogiers ◽  
Ulrika C. Frising ◽  
Soňa Kucharíková ◽  
Mary Ann Jabra-Rizk ◽  
Geert van Loo ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Nlrp3 Inflammasome ◽  
Molecular Mechanisms ◽  
Myeloid Cell ◽  
Opportunistic Pathogen ◽  
Cell Immune Response ◽  
Inflammasome Activation ◽  
Dependent Manner ◽  
Morphological Transformation ◽  
Content Type

ABSTRACT Candida albicans is an opportunistic fungal pathogen that can cause life-threatening infections, particularly in immunocompromised patients. C. albicans induced activation of the Nlrp3 inflammasome, leading to secretion of bioactive interleukin 1β (IL-1β) is a crucial myeloid cell immune response needed for antifungal host defense. Being a pleiomorphic fungus, C. albicans can provoke Nlrp3 inflammasome responses only upon morphological transformation to its hyphal appearance. However, the specific hyphal factors that enable C. albicans to activate the Nlrp3 inflammasome in primary macrophages remain to be revealed. Here, we identify candidalysin, a peptide derived from the hypha-specific ECE1 gene, as a fungal trigger for Nlrp3 inflammasome-mediated maturation and secretion of IL-1β from primary macrophages. Direct peptide administration experiments showed that candidalysin was sufficient for inducing secretion of mature IL-1β from macrophages in an Nlrp3 inflammasome-dependent manner. Conversely, infection experiments using candidalysin-deficient C. albicans showed that candidalysin crucially contributed to the capacity of this fungus to induce maturation and secretion of IL-1β from primary macrophages. These complementary observations identify the expression of candidalysin as one of the molecular mechanisms by which hyphal transformation equips C. albicans with its proinflammatory capacity to elicit the release of bioactive IL-1β from macrophages. IMPORTANCE Candidiasis is a potentially lethal condition that is caused by systemic dissemination of Candida albicans, a common fungal commensal residing mostly on mucosal surfaces. The transition of C. albicans from an innocuous commensal to an opportunistic pathogen goes hand in hand with its morphological transformation from a fungus to a hyphal appearance. On the one hand, the latter manifestation enables C. albicans to penetrate tissues, while on the other hand, the expression of many hypha-specific genes also endows it with the capacity to trigger particular cytokine responses. The Nlrp3 inflammasome is a crucial component of the innate immune system that provokes release of the IL-1β cytokine from myeloid cells upon encountering C. albicans hyphae. Our study reveals the peptide candidalysin as one of the hypha-derived drivers of Nlrp3 inflammasome responses in primary macrophages and, thus, contributes to better understanding the fungal mechanisms that determine the pathogenicity of C. albicans.

scholarly journals Thiostrepton Hijacks Pyoverdine Receptors To Inhibit Growth ofPseudomonas aeruginosa

2019 ◽  
Vol 63 (9) ◽  
Author(s):  
Michael R. M. Ranieri ◽  
Derek C. K. Chan ◽  
Luke N. Yaeger ◽  
Madeleine Rudolph ◽  
Sawyer Karabelas-Pittman ◽  
...  
Keyword(s):  
Biofilm Formation ◽  
Opportunistic Pathogen ◽  
Multidrug Resistant ◽  
Clinical Isolates ◽  
23S Rrna ◽  
Dependent Manner ◽  
Peptide Antibiotics ◽  
Iron Starvation ◽  
Gram Negative ◽  
Content Type

ABSTRACTPseudomonas aeruginosais a biofilm-forming opportunistic pathogen and is intrinsically resistant to many antibiotics. In a high-throughput screen for molecules that modulate biofilm formation, we discovered that the thiopeptide antibiotic thiostrepton (TS), which is considered to be inactive against Gram-negative bacteria, stimulatedP. aeruginosabiofilm formation in a dose-dependent manner. This phenotype is characteristic of exposure to antimicrobial compounds at subinhibitory concentrations, suggesting that TS was active againstP. aeruginosa. Supporting this observation, TS inhibited the growth of a panel of 96 multidrug-resistant (MDR)P. aeruginosaclinical isolates at low-micromolar concentrations. TS also had activity againstAcinetobacter baumanniiclinical isolates. The expression of Tsr, a 23S rRNA-modifying methyltransferase from TS producerStreptomyces azureus, intransconferred TS resistance, confirming that the drug acted via its canonical mode of action, inhibition of ribosome function. The deletion of oligopeptide permease systems used by other peptide antibiotics for uptake failed to confer TS resistance. TS susceptibility was inversely proportional to iron availability, suggesting that TS exploits uptake pathways whose expression is increased under iron starvation. Consistent with this finding, TS activity againstP. aeruginosaandA. baumanniiwas potentiated by the FDA-approved iron chelators deferiprone and deferasirox and by heat-inactivated serum. Screening ofP. aeruginosamutants for TS resistance revealed that it exploits pyoverdine receptors FpvA and FpvB to cross the outer membrane. We show that the biofilm stimulation phenotype can reveal cryptic subinhibitory antibiotic activity, and that TS has activity against select multidrug-resistant Gram-negative pathogens under iron-limited growth conditions, similar to those encountered at sites of infection.

scholarly journals Identification of Clinical Isolates of Candida albicans with Increased Fitness in Colonization of the Murine Gut

2021 ◽  
Vol 7 (9) ◽  
pp. 695
Author(s):  
Rebeca Alonso-Monge ◽  
Daniel Prieto ◽  
Ioana Coman ◽  
Sara Rochas ◽  
David M. Arana ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Opportunistic Pathogen ◽  
Clinical Isolates ◽  
Fungal Colonization ◽  
Phenotypic Analysis ◽  
Bacterial Microbiota ◽  
Specific Trait ◽  
Strain Sc5314 ◽  
Previously Treated

The commensal and opportunistic pathogen Candida albicans is an important cause of fungal diseases in humans, with the gastrointestinal tract being an important reservoir for its infections. The study of the mechanisms promoting the C. albicans commensal state has attracted considerable attention over the last few years, and several studies have focused on the identification of the intestinal human mycobiota and the characterization of Candida genes involved in its establishment as a commensal. In this work, we have barcoded 114 clinical C. albicans isolates to identify strains with an enhanced fitness in a murine gastrointestinal commensalism model. The 114 barcoded clinical isolates were pooled in four groups of 28 to 30 strains that were inoculated by gavage in mice previously treated with antibacterial therapy. Eight strains that either exhibited higher colonization load and/or remained in the gut after antibiotic removal were selected. The phenotypic analysis of these strains compared to an RFP-tagged SC5314 wild type strain did not reveal any specific trait associated with its increased colonization; all strains were able to filament and six of the eight strains displayed invasive growth on Spider medium. Analysis of one of these strains, CaORAL3, revealed that although mice required previous bacterial microbiota reduction with antibiotics to be able to be colonized, removal of this procedure could take place the same day (or even before) Candida inoculation. This strain was able to colonize the intestine of mice already colonized with Candida without antibiotic treatment in co-housing experiments. CaORAL3 was also able to be established as a commensal in mice previously colonized by another (CaHG43) or the same (CaORAL3) C. albicans strain. Therefore, we have identified C. albicans isolates that display higher colonization load than the standard strain SC5314 which will surely facilitate the analysis of the factors that regulate fungal colonization.

scholarly journals Temperature, pH and Trimethoprim-Sulfamethoxazole Are Potent Inhibitors of Biofilm Formation by Stenotrophomonas maltophilia Clinical Isolates

2017 ◽  
Vol 66 (4) ◽  
pp. 433-438 ◽  
Author(s):  
Marjan Biočanin ◽  
Haowa Madi ◽  
Zorica Vasiljević ◽  
Milan Kojić ◽  
Branko Jovčić ◽  
...  
Keyword(s):  
Biofilm Formation ◽  
Stenotrophomonas Maltophilia ◽  
Tertiary Care ◽  
Opportunistic Pathogen ◽  
Growth Conditions ◽  
Clinical Isolates ◽  
Multiple Drug ◽  
Dependent Manner ◽  
Virulence Determinants ◽  
Intrinsic Resistance

Stenotrophomonas maltophilia, an opportunistic pathogen usually connected with healthcare-associated infections, is an environmental bacterium. Intrinsic resistance to multiple antibiotics, with different virulence determinants in the last decade classified this bacterium in the group of global multiple drug resistant (MDR) organism. S. maltophilia clinical isolates, were collected from tertiary care pediatric hospital in Belgrade, Serbia to investigate influence of different factors on biofilm formation, kinetics of biofilm formation for strong biofilm producers and effect of trimethoprim-sulfamethoxazole (TMP/SMX) on formed biofilm. Most of the isolates (89.8%) were able to form a biofilm. Analysis of biofilm formation in different growth conditions showed that changing of temeperature and pH had the stronggest effect on biofilm formation almost equally in group of cystic fibrosis (CF) and non-CF strains. TMP/SMX in concentration of 50 μg/ml reduced completely 24 h old biofilms while concentration of 25 μg/ml effects formed biofilms in a strain dependent manner. Among strains able to form strong biofilm CF isolates formed biofilm slower than non-CF isolates, while shaking conditions did not affect biofilm formation. Swimming motility was detected in both CF and non-CF isolates, however more motile strain formed stronger biofilms. This study suggests that temperature, pH and TMP/SMX had the strongest influence on biofilm formation in analyzed collection of S. maltophilia. A positive correlation between motility and strength of formed biofilm was demonstrated.

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 Activation of Cph1 causes ß(1,3)-glucan unmasking in Candida albicans and attenuates virulence in mice in a neutrophil-dependent manner

2021 ◽  
Vol 17 (8) ◽  
pp. e1009839
Author(s):  
Andrew S. Wagner ◽  
Trevor J. Hancock ◽  
Stephen W. Lumsdaine ◽  
Sarah J. Kauffman ◽  
Mikayla M. Mangrum ◽  
...  
Keyword(s):  
Cell Wall ◽  
Transcription Factor ◽  
Candida Albicans ◽  
Immune System ◽  
Mapk Pathway ◽  
Host Immune System ◽  
Dependent Manner ◽  
Antibody Treatment ◽  
Fungal Burden ◽  
Upstream Kinase

Masking the immunogenic cell wall epitope ß(1,3)-glucan under an outer layer of mannosylated glycoproteins is an important virulence factor deployed by Candida albicans during infection. Consequently, increased ß(1,3)-glucan exposure (unmasking) reveals C. albicans to the host’s immune system and attenuates its virulence. We have previously shown that activation of the Cek1 MAPK pathway via expression of a hyperactive allele of an upstream kinase (STE11ΔN467) induces unmasking. It also increased survival of mice in a murine disseminated candidiasis model and attenuated kidney fungal burden by ≥33 fold. In this communication, we utilized cyclophosphamide-induced immunosuppression to test if the clearance of the unmasked STE11ΔN467 mutant was dependent on the host immune system. Suppression of the immune response by cyclophosphamide reduced the attenuation in fungal burden caused by the STE11ΔN467 allele. Moreover, specific depletion of neutrophils via 1A8 antibody treatment also reduced STE11ΔN467-dependent fungal burden attenuation, but to a lesser extent than cyclophosphamide, demonstrating an important role for neutrophils in mediating fungal clearance of unmasked STE11ΔN467 cells. In an effort to understand the mechanism by which Ste11ΔN467 causes unmasking, transcriptomics were used to reveal that several components in the Cek1 MAPK pathway were upregulated, including the transcription factor CPH1 and the cell wall sensor DFI1. In this report we show that a cph1ΔΔ mutation restored ß(1,3)-glucan exposure to wild-type levels in the STE11ΔN467 strain, confirming that Cph1 is the transcription factor mediating Ste11ΔN467-induced unmasking. Furthermore, Cph1 is shown to induce a positive feedback loop that increases Cek1 activation. In addition, full unmasking by STE11ΔN467 is dependent on the upstream cell wall sensor DFI1. However, while deletion of DFI1 significantly reduced Ste11ΔN467-induced unmasking, it did not impact activation of the downstream kinase Cek1. Thus, it appears that once stimulated by Ste11ΔN467, Dfi1 activates a parallel signaling pathway that is involved in Ste11ΔN467-induced unmasking.

scholarly journals Photodynamic Therapy by Diaryl-Porphyrins to Control the Growth of Candida albicans

Cosmetics ◽  
2020 ◽  
Vol 7 (2) ◽  
pp. 31
Author(s):  
Viviana Teresa Orlandi ◽  
Eleonora Martegani ◽  
Fabrizio Bolognese ◽  
Nicola Trivellin ◽  
Olga Maťátková ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Photodynamic Therapy ◽  
Opportunistic Pathogen ◽  
Light Sources ◽  
Dependent Manner ◽  
Photodynamic Treatment ◽  
Body Tissues ◽  
The Family ◽  
Athlete’S Foot ◽  
Dose Dependent

Candida albicans is an opportunistic pathogen that often causes skin infections such as oral thrush, nail fungus, athlete’s foot, and diaper rash. Under particular conditions, C. albicans alters the natural balance of the host microbiota, and as a result, the skin or its accessory structures lose their function and appearance. Conventional antimycotic drugs are highly toxic to host tissues, and long-lasting drug administration induces the arising of resistant strains that make the antimycotic therapy ineffective. Among new antimicrobial approaches to combine with traditional drugs, light-based techniques are very promising. In this study, a panel of dyes was considered for photodynamic therapy (PDT) applications to control the growth of the model strain C. albicans ATCC 14053. The chosen photosensitizers (PSs) belong to the family of synthetic porphyrins, and in particular, they are diaryl-porphyrins. Among these, two monocationic PSs were shown to be particularly efficient in killing C. albicans upon irradiation with light at 410 nm, in a light-dose-dependent manner. The elicited photo-oxidative stress induced the loss of the internal cellular architecture and death. The photodynamic treatment was also successful in inhibiting the biofilm formation of clinical C. albicans strains. In conclusion, this study supports the great potential of diaryl-porphyrins in antimicrobial PDT to control the growth of yeasts on body tissues easily reachable by light sources, such as skin and oral cavity.

scholarly journals Glycerol Is Metabolized in a Complex and Strain-Dependent Manner in Enterococcus faecalis

2009 ◽  
Vol 192 (3) ◽  
pp. 779-785 ◽  
Author(s):  
Alain Bizzini ◽  
Chen Zhao ◽  
Aurélie Budin-Verneuil ◽  
Nicolas Sauvageot ◽  
Jean-Christophe Giard ◽  
...  
Keyword(s):  
Gene Expression ◽  
Enterococcus Faecalis ◽  
Glycerol Dehydrogenase ◽  
Dihydroxyacetone Phosphate ◽  
Dependent Manner ◽  
Anaerobic Conditions ◽  
Dihydroxyacetone Kinase ◽  
Aerobic And Anaerobic ◽  
Strain Dependent ◽  
Aerobic And Anaerobic Conditions

ABSTRACT Enterococcus faecalis is equipped with two pathways of glycerol dissimilation. Glycerol can either first be phosphorylated by glycerol kinase and then oxidized by glycerol-3-phosphate oxidase (the glpK pathway) or first be oxidized by glycerol dehydrogenase and then phosphorylated by dihydroxyacetone kinase (the dhaK pathway). Both pathways lead to the formation of dihydroxyacetone phosphate, an intermediate of glycolysis. It was assumed that the glpK pathway operates during aerobiosis and that the dhaK pathway operates under anaerobic conditions. Because this had not been analyzed by a genetic study, we constructed mutants of strain JH2-2 affected in both pathways. The growth of these mutants on glycerol under aerobic and anaerobic conditions was monitored. In contrast to the former model, results strongly suggest that glycerol is catabolized simultaneously by both pathways in the E. faecalis JH2-2 strain in the presence of oxygen. In accordance with the former model, glycerol is metabolized by the dhaK pathway under anaerobic conditions. Comparison of different E. faecalis isolates revealed an impressive diversity of growth behaviors on glycerol. Analysis by BLAST searching and real-time reverse transcriptase PCR revealed that this diversity is based not on different gene contents but rather on differences in gene expression. Some strains used preferentially the glpK pathway whereas others probably exclusively the dhaK pathway under aerobic conditions. Our results demonstrate that the species E. faecalis cannot be represented by only one model of aerobic glycerol catabolism.

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