Slavena Vylkova, PhD

Manager, Scientific Communications

M_MED-CORE-GAST-GEN

+1 415 514-7869

Custom People Group

Dr. Slavena Vylkova manages the scientific communications for the Benioff Center for Microbiome Medicine (BCMM). Her responsibilities include assisting with pre-award research funding operations, scientific writing/editing and project development.
Previously, Slavena was a research assistant professor at Friedrich Schiller University in Jena, Germany, where she led a research group focusing on the molecular basis of metabolic adaptation of the fungal pathogen Candida albicans to the host niches and associated microbiota. She received her PhD in Oral Biology from State University of New York at Buffalo with Dr. Mira Edgerton and her postdoctoral training in Dr. Michael Lorenz's laboratory in McGovern Medical School in Houston, TX.

Publications

Synergistic cross-kingdom host cell damage between Candida albicans and Enterococcus faecalis.

bioRxiv : the preprint server for biology

Kapitan M, Niemiec MJ, Millet N, Brandt P, Chowdhury MEK, Czapka A, Abdissa K, Hoffmann F, Lange A, Veleba M, Nietzsche S, Mosig AS, Löffler B, Marquet M, Makarewicz O, Kline KA, Vylkova S, Swidergall M, Jacobsen ID

A highly conserved tRNA modification contributes to C. albicans filamentation and virulence.

Microbiology spectrum

Böttcher B, Kienast SD, Leufken J, Eggers C, Sharma P, Leufken CM, Morgner B, Drexler HCA, Schulz D, Allert S, Jacobsen ID, Vylkova S, Leidel SA, Brunke S

Escherichia coli Nissle 1917 Antagonizes Candida albicans Growth and Protects Intestinal Cells from C. albicans-Mediated Damage.

Microorganisms

Rebai Y, Wagner L, Gnaien M, Hammer ML, Kapitan M, Niemiec MJ, Mami W, Mosbah A, Messadi E, Mardassi H, Vylkova S, Jacobsen ID, Znaidi S

Pathogen-specific innate immune response patterns are distinctly affected by genetic diversity.

Nature communications

Häder A, Schäuble S, Gehlen J, Thielemann N, Buerfent BC, Schüller V, Hess T, Wolf T, Schröder J, Weber M, Hünniger K, Löffler J, Vylkova S, Panagiotou G, Schumacher J, Kurzai O

High-Throughput Profiling of Candida auris Isolates Reveals Clade-Specific Metabolic Differences.

Microbiology spectrum

Brandt P, Mirhakkak MH, Wagner L, Driesch D, Möslinger A, Fänder P, Schäuble S, Panagiotou G, Vylkova S

Integrated analysis of SR-like protein kinases Sky1 and Sky2 links signaling networks with transcriptional regulation in Candida albicans.

Frontiers in cellular and infection microbiology

Luther CH, Brandt P, Vylkova S, Dandekar T, Müller T, Dittrich M

Functional analysis of the Candida albicans ECE1 Promoter.

Microbiology spectrum

Garbe E, Thielemann N, Hohner S, Kumar A, Vylkova S, Kurzai O, Martin R

Systematic Metabolic Profiling Identifies De Novo Sphingolipid Synthesis as Hypha Associated and Essential for Candida albicans Filamentation.

mSystems

Garbe E, Gerwien F, Driesch D, Müller T, Böttcher B, Gräler M, Vylkova S

Impaired amino acid uptake leads to global metabolic imbalance of Candida albicans biofilms.

NPJ biofilms and microbiomes

Böttcher B, Driesch D, Krüger T, Garbe E, Gerwien F, Kniemeyer O, Brakhage AA, Vylkova S

Lactobacillus rhamnosus colonisation antagonizes Candida albicans by forcing metabolic adaptations that compromise pathogenicity.

Nature communications

Alonso-Roman R, Last A, Mirhakkak MH, Sprague JL, Möller L, Großmann P, Graf K, Gratz R, Mogavero S, Vylkova S, Panagiotou G, Schäuble S, Hube B, Gresnigt MS

Candida albicans SR-Like Protein Kinases Regulate Different Cellular Processes: Sky1 Is Involved in Control of Ion Homeostasis, While Sky2 Is Important for Dipeptide Utilization.

Frontiers in cellular and infection microbiology

Brandt P, Gerwien F, Wagner L, Krüger T, Ramírez-Zavala B, Mirhakkak MH, Schäuble S, Kniemeyer O, Panagiotou G, Brakhage AA, Morschhäuser J, Vylkova S

GNP2 Encodes a High-Specificity Proline Permease in Candida albicans.

mBio

Garbe E, Miramón P, Gerwien F, Ueberschaar N, Hansske-Braun L, Brandt P, Böttcher B, Lorenz M, Vylkova S

Metabolic modeling predicts specific gut bacteria as key determinants for Candida albicans colonization levels.

The ISME journal

Mirhakkak MH, Schäuble S, Klassert TE, Brunke S, Brandt P, Loos D, Uribe RV, Senne de Oliveira Lino F, Ni Y, Vylkova S, Slevogt H, Hube B, Weiss GJ, Sommer MOA, Panagiotou G

Active neutrophil responses counteract Candida albicans burn wound infection of ex vivo human skin explants.

Scientific reports

von Müller C, Bulman F, Wagner L, Rosenberger D, Marolda A, Kurzai O, Eißmann P, Jacobsen ID, Perner B, Hemmerich P, Vylkova S

Bloodstream infection due to Enterobacter ludwigii, correlating with massive aggregation on the surface of a central venous catheter.

Infection

Wagner L, Bloos F, Vylkova S

Catch the wave: Metabolomic analyses in human pathogenic fungi.

PLoS pathogens

Brandt P, Garbe E, Vylkova S

Clinical Candida albicans Vaginal Isolates and a Laboratory Strain Show Divergent Behaviors during Macrophage Interactions.

mSphere

Gerwien F, Dunker C, Brandt P, Garbe E, Jacobsen ID, Vylkova S

Modulation of phagosomal pH by Candida albicans promotes hyphal morphogenesis and requires Stp2p, a regulator of amino acid transport.

PLoS pathogens

Vylkova S, Lorenz MC

Histatin 5 initiates osmotic stress response in Candida albicans via activation of the Hog1 mitogen-activated protein kinase pathway.

Eukaryotic cell

Vylkova S, Jang WS, Li W, Nayyar N, Edgerton M

The role of released ATP in killing Candida albicans and other extracellular microbial pathogens by cationic peptides.

Purinergic signalling

Vylkova S, Sun JN, Edgerton M

Human beta-defensins kill Candida albicans in an energy-dependent and salt-sensitive manner without causing membrane disruption.

Antimicrobial agents and chemotherapy

Vylkova S, Nayyar N, Li W, Edgerton M

Distinct antifungal mechanisms: beta-defensins require Candida albicans Ssa1 protein, while Trk1p mediates activity of cysteine-free cationic peptides.

Antimicrobial agents and chemotherapy

Vylkova S, Li XS, Berner JC, Edgerton M

The TRK1 potassium transporter is the critical effector for killing of Candida albicans by the cationic protein, Histatin 5.

The Journal of biological chemistry

Baev D, Rivetta A, Vylkova S, Sun JN, Zeng GF, Slayman CL, Edgerton M

Calcium blocks fungicidal activity of human salivary histatin 5 through disruption of binding with Candida albicans.

Journal of dental research

Dong J, Vylkova S, Li XS, Edgerton M

Killing of Candida albicans by human salivary histatin 5 is modulated, but not determined, by the potassium channel TOK1.

Infection and immunity

Baev D, Rivetta A, Li XS, Vylkova S, Bashi E, Slayman CL, Edgerton M

Publications

Synergistic cross-kingdom host cell damage between Candida albicans and Enterococcus faecalis.

A highly conserved tRNA modification contributes to C. albicans filamentation and virulence.

Escherichia coli Nissle 1917 Antagonizes Candida albicans Growth and Protects Intestinal Cells from C. albicans-Mediated Damage.

Pathogen-specific innate immune response patterns are distinctly affected by genetic diversity.

High-Throughput Profiling of Candida auris Isolates Reveals Clade-Specific Metabolic Differences.

Integrated analysis of SR-like protein kinases Sky1 and Sky2 links signaling networks with transcriptional regulation in Candida albicans.

Functional analysis of the Candida albicans ECE1 Promoter.

Systematic Metabolic Profiling Identifies De Novo Sphingolipid Synthesis as Hypha Associated and Essential for Candida albicans Filamentation.

Impaired amino acid uptake leads to global metabolic imbalance of Candida albicans biofilms.

Lactobacillus rhamnosus colonisation antagonizes Candida albicans by forcing metabolic adaptations that compromise pathogenicity.

Candida albicans SR-Like Protein Kinases Regulate Different Cellular Processes: Sky1 Is Involved in Control of Ion Homeostasis, While Sky2 Is Important for Dipeptide Utilization.

GNP2 Encodes a High-Specificity Proline Permease in Candida albicans.

Metabolic modeling predicts specific gut bacteria as key determinants for Candida albicans colonization levels.

Active neutrophil responses counteract Candida albicans burn wound infection of ex vivo human skin explants.

Bloodstream infection due to Enterobacter ludwigii, correlating with massive aggregation on the surface of a central venous catheter.

Catch the wave: Metabolomic analyses in human pathogenic fungi.

Clinical Candida albicans Vaginal Isolates and a Laboratory Strain Show Divergent Behaviors during Macrophage Interactions.

The Transcription Factor Stp2 Is Important for Candida albicans Biofilm Establishment and Sustainability.

Ahr1 and Tup1 Contribute to the Transcriptional Control of Virulence-Associated Genes in Candida albicans.

Environmental pH modulation by pathogenic fungi as a strategy to conquer the host.

Phagosomal Neutralization by the Fungal Pathogen Candida albicans Induces Macrophage Pyroptosis.

Robust Extracellular pH Modulation by Candida albicans during Growth in Carboxylic Acids.

Modulation of phagosomal pH by Candida albicans promotes hyphal morphogenesis and requires Stp2p, a regulator of amino acid transport.

The fungal pathogen Candida albicans autoinduces hyphal morphogenesis by raising extracellular pH.

Conservation and dispersion of sequence and function in fungal TRK potassium transporters: focus on Candida albicans.

Role of acetyl coenzyme A synthesis and breakdown in alternative carbon source utilization in Candida albicans.

Histatin 5 initiates osmotic stress response in Candida albicans via activation of the Hog1 mitogen-activated protein kinase pathway.

The role of released ATP in killing Candida albicans and other extracellular microbial pathogens by cationic peptides.

Human beta-defensins kill Candida albicans in an energy-dependent and salt-sensitive manner without causing membrane disruption.

Distinct antifungal mechanisms: beta-defensins require Candida albicans Ssa1 protein, while Trk1p mediates activity of cysteine-free cationic peptides.

The TRK1 potassium transporter is the critical effector for killing of Candida albicans by the cationic protein, Histatin 5.

Calcium blocks fungicidal activity of human salivary histatin 5 through disruption of binding with Candida albicans.

Killing of Candida albicans by human salivary histatin 5 is modulated, but not determined, by the potassium channel TOK1.