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1. The hyphal-specific toxin candidalysin promotes fungal gut commensalism

Author

Liang, Shen-Huan, Sircaik, Shabnam, Dainis, Joseph, Kakade, Pallavi, Penumutchu, Swathi, McDonough, Liam D., Chen, Ying-Han, Frazer, Corey, Schille, Tim B., Allert, Stefanie, Elshafee, Osama, Hänel, Maria, Mogavero, Selene, Vaishnava, Shipra, Cadwell, Ken, Belenky, Peter, Perez, J. Christian, Hube, Bernhard, Ene, Iuliana V., and Bennett, Richard J.

Published
2024
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2. Candida albicans translocation through the intestinal epithelial barrier is promoted by fungal zinc acquisition and limited by NFκB-mediated barrier protection

Author

Sprague, Jakob L., primary, Schille, Tim B., additional, Allert, Stefanie, additional, Trümper, Verena, additional, Lier, Adrian, additional, Großmann, Peter, additional, Priest, Emily L., additional, Tsavou, Antzela, additional, Panagiotou, Gianni, additional, Naglik, Julian R., additional, Wilson, Duncan, additional, Schäuble, Sascha, additional, Kasper, Lydia, additional, and Hube, Bernhard, additional

Published
2024
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3. Nanobody-mediated neutralization of candidalysin prevents epithelial damage and inflammatory responses that drive vulvovaginal candidiasis pathogenesis

Author

Valentine, Marisa, primary, Rudolph, Paul, additional, Dietschmann, Axel, additional, Tsavou, Antzela, additional, Mogavero, Selene, additional, Lee, Sejeong, additional, Priest, Emily L., additional, Zhurgenbayeva, Gaukhar, additional, Jablonowski, Nadja, additional, Timme, Sandra, additional, Eggeling, Christian, additional, Allert, Stefanie, additional, Dolk, Edward, additional, Naglik, Julian R., additional, Figge, Marc T., additional, Gresnigt, Mark S., additional, and Hube, Bernhard, additional

Published
2024
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4. Candidalysin Is the Hemolytic Factor of Candida albicans

Author

Mogavero, Selene, primary, Höfs, Sarah, additional, Lauer, Alexa N., additional, Müller, Rita, additional, Brunke, Sascha, additional, Allert, Stefanie, additional, Gerwien, Franziska, additional, Groth, Sabrina, additional, Dolk, Edward, additional, Wilson, Duncan, additional, Gutsmann, Thomas, additional, and Hube, Bernhard, additional

Published
2022
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7. Cover Image: Candidalysin delivery to the invasion pocket is critical for host epithelial damage induced by Candida albicans (Cellular Microbiology 10/2021)

Author

Mogavero, Selene, primary, Sauer, Frank M., additional, Brunke, Sascha, additional, Allert, Stefanie, additional, Schulz, Daniela, additional, Wisgott, Stephanie, additional, Jablonowski, Nadja, additional, Elshafee, Osama, additional, Krüger, Thomas, additional, Kniemeyer, Olaf, additional, Brakhage, Axel A., additional, Naglik, Julian R., additional, Dolk, Edward, additional, and Hube, Bernhard, additional

Published
2021
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8. A variant ECE1 allele contributes to reduced pathogenicity of Candida albicans during vulvovaginal candidiasis

Author

Liu, Junyan, primary, Willems, Hubertine M. E., additional, Sansevere, Emily A., additional, Allert, Stefanie, additional, Barker, Katherine S., additional, Lowes, David J., additional, Dixson, Andrew C., additional, Xu, Zhenbo, additional, Miao, Jian, additional, DeJarnette, Christian, additional, Tournu, Helene, additional, Palmer, Glen E., additional, Richardson, Jonathan P., additional, Barrera, Francisco N., additional, Hube, Bernhard, additional, Naglik, Julian R., additional, and Peters, Brian M., additional

Published
2021
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9. Candidalysin delivery to the invasion pocket is critical for host epithelial damage induced by Candida albicans

Author

Mogavero, Selene, primary, Sauer, Frank M., additional, Brunke, Sascha, additional, Allert, Stefanie, additional, Schulz, Daniela, additional, Wisgott, Stephanie, additional, Jablonowski, Nadja, additional, Elshafee, Osama, additional, Krüger, Thomas, additional, Kniemeyer, Olaf, additional, Brakhage, Axel A., additional, Naglik, Julian R., additional, Dolk, Edward, additional, and Hube, Bernhard, additional

Published
2021
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10. Survival Strategies of Pathogenic Candida Species in Human Blood Show Independent and Specific Adaptations

Author

Kämmer, Philipp, primary, McNamara, Sylvie, additional, Wolf, Thomas, additional, Conrad, Theresia, additional, Allert, Stefanie, additional, Gerwien, Franziska, additional, Hünniger, Kerstin, additional, Kurzai, Oliver, additional, Guthke, Reinhard, additional, Hube, Bernhard, additional, Linde, Jörg, additional, and Brunke, Sascha, additional

Published
2020
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13. Candida albicans-Induced Epithelial Damage Mediates Translocation through Intestinal Barriers

Author

Allert, Stefanie, primary, Förster, Toni M., additional, Svensson, Carl-Magnus, additional, Richardson, Jonathan P., additional, Pawlik, Tony, additional, Hebecker, Betty, additional, Rudolphi, Sven, additional, Juraschitz, Marc, additional, Schaller, Martin, additional, Blagojevic, Mariana, additional, Morschhäuser, Joachim, additional, Figge, Marc Thilo, additional, Jacobsen, Ilse D., additional, Naglik, Julian R., additional, Kasper, Lydia, additional, Mogavero, Selene, additional, and Hube, Bernhard, additional

Published
2018
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16. The Snf1-activating kinase Sak1 is a key regulator of metabolic adaptation and in vivo fitness of Candida albicans.

Author

Ramírez‐Zavala, Bernardo, Mottola, Austin, Haubenreißer, Julia, Schneider, Sabrina, Allert, Stefanie, Brunke, Sascha, Ohlsen, Knut, Hube, Bernhard, and Morschhäuser, Joachim

Subjects
CANDIDA albicans, BACTERIAL genetics, PHENOTYPIC plasticity, COLONIZATION (Ecology), GENE expression in bacteria
Abstract

The metabolic flexibility of the opportunistic fungal pathogen Candida albicans is important for colonisation and infection of different host niches. Complex regulatory networks, in which protein kinases play central roles, link metabolism and other virulence-associated traits, such as filamentous growth and stress resistance, and thereby control commensalism and pathogenicity. By screening a protein kinase deletion mutant library that was generated in the present work using an improved SAT1 flipper cassette, we found that the previously uncharacterised kinase Sak1 is a key upstream activator of the protein kinase Snf1, a highly conserved regulator of nutrient stress responses that is essential for viability in C. albicans. The sak1Δ mutants failed to grow on many alternative carbon sources and were hypersensitive to cell wall/membrane stress. These phenotypes were mirrored in mutants lacking other subunits of the SNF1 complex and partially compensated by a hyperactive form of Snf1. Transcriptional profiling of sak1Δ mutants showed that Sak1 ensures basal expression of glyoxylate cycle and gluconeogenesis genes even in glucose-rich media and thereby contributes to the metabolic plasticity of C. albicans. In a mouse model of gastrointestinal colonisation, sak1Δ mutants were rapidly outcompeted by wild-type cells, demonstrating that Sak1 is essential for the in vivo fitness of C. albicans. [ABSTRACT FROM AUTHOR]

Published
2017
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17. Identification of Candida glabrata Genes Involved in pH Modulation and Modification of the Phagosomal Environment in Macrophages

Author

Kasper, Lydia, primary, Seider, Katja, additional, Gerwien, Franziska, additional, Allert, Stefanie, additional, Brunke, Sascha, additional, Schwarzmüller, Tobias, additional, Ames, Lauren, additional, Zubiria-Barrera, Cristina, additional, Mansour, Michael K., additional, Becken, Ulrike, additional, Barz, Dagmar, additional, Vyas, Jatin M., additional, Reiling, Norbert, additional, Haas, Albert, additional, Haynes, Ken, additional, Kuchler, Karl, additional, and Hube, Bernhard, additional

Published
2014
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18. Immune Evasion, Stress Resistance, and Efficient Nutrient Acquisition Are Crucial for Intracellular Survival of Candida glabrata within Macrophages

Author

Seider, Katja, primary, Gerwien, Franziska, additional, Kasper, Lydia, additional, Allert, Stefanie, additional, Brunke, Sascha, additional, Jablonowski, Nadja, additional, Schwarzmüller, Tobias, additional, Barz, Dagmar, additional, Rupp, Steffen, additional, Kuchler, Karl, additional, and Hube, Bernhard, additional

Published
2014
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20. Identification of Candida glabrata Genes Involved in pH Modulation and Modification of the Phagosomal Environment in Macrophages.

Author

Kasper, Lydia, Seider, Katja, Gerwien, Franziska, Allert, Stefanie, Brunke, Sascha, Schwarzmüller, Tobias, Ames, Lauren, Zubiria-Barrera, Cristina, Mansour, Michael K., Becken, Ulrike, Barz, Dagmar, Vyas, Jatin M., Reiling, Norbert, Haas, Albert, Haynes, Ken, Kuchler, Karl, and Hube, Bernhard

Subjects
CANDIDA, HYDROGEN-ion concentration, MACROPHAGES, INVASIVE candidiasis, ENDOSOMES, CELL differentiation, CELLULAR signal transduction
Abstract

Candida glabrata currently ranks as the second most frequent cause of invasive candidiasis. Our previous work has shown that C. glabrata is adapted to intracellular survival in macrophages and replicates within non-acidified late endosomal-stage phagosomes. In contrast, heat killed yeasts are found in acidified matured phagosomes. In the present study, we aimed at elucidating the processes leading to inhibition of phagosome acidification and maturation. We show that phagosomes containing viable C. glabrata cells do not fuse with pre-labeled lysosomes and possess low phagosomal hydrolase activity. Inhibition of acidification occurs independent of macrophage type (human/murine), differentiation (M1-/M2-type) or activation status (vitamin D3 stimulation). We observed no differential activation of macrophage MAPK or NFκB signaling cascades downstream of pattern recognition receptors after internalization of viable compared to heat killed yeasts, but Syk activation decayed faster in macrophages containing viable yeasts. Thus, delivery of viable yeasts to non-matured phagosomes is likely not triggered by initial recognition events via MAPK or NFκB signaling, but Syk activation may be involved. Although V-ATPase is abundant in C. glabrata phagosomes, the influence of this proton pump on intracellular survival is low since blocking V-ATPase activity with bafilomycin A1 has no influence on fungal viability. Active pH modulation is one possible fungal strategy to change phagosome pH. In fact, C. glabrata is able to alkalinize its extracellular environment, when growing on amino acids as the sole carbon source in vitro. By screening a C. glabrata mutant library we identified genes important for environmental alkalinization that were further tested for their impact on phagosome pH. We found that the lack of fungal mannosyltransferases resulted in severely reduced alkalinization in vitro and in the delivery of C. glabrata to acidified phagosomes. Therefore, protein mannosylation may play a key role in alterations of phagosomal properties caused by C. glabrata. [ABSTRACT FROM AUTHOR]

Published
2014
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21. Immune Evasion, Stress Resistance, and Efficient Nutrient Acquisition Are Crucial for Intracellular Survival of Candida glabratawithin Macrophages

Author

Seider, Katja, Gerwien, Franziska, Kasper, Lydia, Allert, Stefanie, Brunke, Sascha, Jablonowski, Nadja, Schwarzmüller, Tobias, Barz, Dagmar, Rupp, Steffen, Kuchler, Karl, and Hube, Bernhard

Abstract

ABSTRACTCandida glabratais both a human fungal commensal and an opportunistic pathogen which can withstand activities of the immune system. For example, C. glabratacan survive phagocytosis and replicates within macrophages. However, the mechanisms underlying intracellular survival remain unclear. In this work, we used a functional genomic approach to identify C. glabratadeterminants necessary for survival within human monocyte-derived macrophages by screening a set of 433 deletion mutants. We identified 23 genes which are required to resist killing by macrophages. Based on homologies to Saccharomyces cerevisiaeorthologs, these genes are putatively involved in cell wall biosynthesis, calcium homeostasis, nutritional and stress response, protein glycosylation, or iron homeostasis. Mutants were further characterized using a series of in vitroassays to elucidate the genes' functions in survival. We investigated different parameters of C. glabrata-phagocyte interactions: uptake by macrophages, replication within macrophages, phagosomal pH, and recognition of mutant cells by macrophages as indicated by production of reactive oxygen species and tumor necrosis factor alpha (TNF-a). We further studied the cell surface integrity of mutant cells, their ability to grow under nutrient-limited conditions, and their susceptibility to stress conditions mirroring the harsh environment inside a phagosome. Additionally, resistance to killing by neutrophils was analyzed. Our data support the view that immune evasion is a key aspect of C. glabratavirulence and that increased immune recognition causes increased antifungal activities by macrophages. Furthermore, stress resistance and efficient nutrient acquisition, in particular, iron uptake, are crucial for intraphagosomal survival of C. glabrata.

Published
2013
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22. Survival Strategies of Pathogenic CandidaSpecies in Human Blood Show Independent and Specific Adaptations

Author

Kämmer, Philipp, McNamara, Sylvie, Wolf, Thomas, Conrad, Theresia, Allert, Stefanie, Gerwien, Franziska, Hünniger, Kerstin, Kurzai, Oliver, Guthke, Reinhard, Hube, Bernhard, Linde, Jörg, and Brunke, Sascha

Abstract

To ensure their survival, pathogens have to adapt immediately to new environments in their hosts, for example, during the transition from the gut to the bloodstream. Here, we investigated the basis of this adaptation in a group of fungal species which are among the most common causes of hospital-acquired infections, the Candidaspecies. On the basis of a human whole-blood infection model, we studied which genes and processes are active over the course of an infection in both the host and four different Candidapathogens. Remarkably, we found that, while the human host response during the early phase of infection is predominantly uniform, the pathogens pursue largely individual strategies and each one regulates genes involved in largely disparate processes in the blood. Our results reveal that C. albicans, C. glabrata, C. parapsilosis, and C. tropicalisall have developed individual strategies for survival in the host. This indicates that their pathogenicity in humans has evolved several times independently and that genes which are central for survival in the host for one species may be irrelevant in another.

Published
2020
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23. A highly conserved tRNA modification contributes to C. albicans filamentation and virulence.

Author

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, and Brunke S

Subjects
Virulence genetics, Humans, Animals, Candida pathogenicity, Candida genetics, Candida metabolism, Host-Pathogen Interactions, Mice, Epithelial Cells microbiology, Candida albicans genetics, Candida albicans pathogenicity, Candida albicans metabolism, RNA, Transfer genetics, RNA, Transfer metabolism, Fungal Proteins genetics, Fungal Proteins metabolism, Candidiasis microbiology, Hyphae growth & development, Hyphae genetics, Hyphae metabolism
Abstract

tRNA modifications play important roles in maintaining translation accuracy in all domains of life. Disruptions in the tRNA modification machinery, especially of the anticodon stem loop, can be lethal for many bacteria and lead to a broad range of phenotypes in baker's yeast. Very little is known about the function of tRNA modifications in host-pathogen interactions, where rapidly changing environments and stresses require fast adaptations. We found that two closely related fungal pathogens of humans, the highly pathogenic Candida albicans and its much less pathogenic sister species, Candida dubliniensis , differ in the function of a tRNA-modifying enzyme. This enzyme, Hma1, exhibits species-specific effects on the ability of the two fungi to grow in the hypha morphology, which is central to their virulence potential. We show that Hma1 has tRNA-threonylcarbamoyladenosine dehydratase activity, and its deletion alters ribosome occupancy, especially at 37°C-the body temperature of the human host. A C. albicans HMA1 deletion mutant also shows defects in adhesion to and invasion into human epithelial cells and shows reduced virulence in a fungal infection model. This links tRNA modifications to host-induced filamentation and virulence of one of the most important fungal pathogens of humans.IMPORTANCEFungal infections are on the rise worldwide, and their global burden on human life and health is frequently underestimated. Among them, the human commensal and opportunistic pathogen, Candida albicans, is one of the major causative agents of severe infections. Its virulence is closely linked to its ability to change morphologies from yeasts to hyphae. Here, this ability is linked-to our knowledge for the first time-to modifications of tRNA and translational efficiency. One tRNA-modifying enzyme, Hma1, plays a specific role in C. albicans and its ability to invade the host. This adds a so-far unknown layer of regulation to the fungal virulence program and offers new potential therapeutic targets to fight fungal infections., Competing Interests: The authors declare no conflict of interest.

Published
2024
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