Nutrient acquisition in infections
In order to survive and replicate within the host, pathogens, such as pathogenic Candida species, need to obtain nutrients during infections. The host, on the other hand, attempts to withhold these nutrients from the pathogen as much as possible (“nutritional immunity”). A molecular tug-of-war starts, where both sides try to sequester essential micronutrients, for example iron or zinc, and get hold of carbon and nitrogen sources. The outcome of any infection is in large parts determined by this struggle, and understanding the mechanisms behind it will help finding novel ways to fight pathogens.
We are interested in the regulation of the fungal response to low micro- and macronutrient levels, which will be encountered by Candida cells in the host. Iron is an essential metal for almost all organisms and iron acquisition within a host is a prerequisite for any type of infection. For this reason, we are investigating the iron uptake systems, and their regulation, in both C. albicans and C. glabrata. Zinc, as a central cofactor in many proteins, is of similar importance, and our research focuses on the zinc acquisition systems Candida species have at their disposal. Finally, as an example of a macronutrient which fungi need to grow, we are investigating the nitrogen sources used by C. albicans during infections.
(2021) The involvement of the Candida glabrata trehalase enzymes in stress resistance and gut colonization. Virulence 12(1), 329-345.
(2020) Candidalysin is a potent trigger of alarmin and antimicrobial peptide release in epithelial cells. Cells 9(3), 699.
(2020) Ahr1 and Tup1 contribute to the transcriptional control of virulence-associated genes in Candida albicans. mBio 11(2), e00206-20.
(2020) Lysosome fusion maintains phagosome integrity during fungal infection. Cell Host Microbe 28(6), 798-812.
(2019) Recent trends in molecular diagnostics of yeast infections: from PCR to NGS. FEMS Microbiol Rev 43(5), 517-547. (Review)
(2019) The Candida albicans exotoxin Candidalysin promotes alcohol-associated liver disease. J Hepatol 72(3), 391-400.
(2019) Cooperative role of MAPK pathways in the interaction of Candida albicans with the host Epithelium. Microorganisms 8(1), 48.
(2019) Disruption of membrane integrity by the bacteria-derived antifungal jagaricin. Antimicrob Agents Chemother 63(9), e00707-19.
(2019) Candidalysin activates innate epithelial immune responses via epidermal growth factor receptor. Nat Commun 10(1), 2297.
(2019) Effects of histatin 5 modifications on antifungal activity and kinetics of proteolysis. Protein Sci 29(2), 480-493.
(2019) RNAi as a tool to study virulence in the pathogenic yeast Candida glabrata. Front Microbiol 10, 1679.
(2019) Candidalysin: Discovery and function in Candida albicans infections. Curr Opin Microbiol 52, 100-109. (Review)
(2019) Host-pathogen interactions during female genital tract infections. Trends Microbiol 27(12), 982-996. (Review)
(2019) Candidalysin is required for neutrophil recruitment and virulence during systemic Candida albicans infection. J Infect Dis 220(9), 1477-1488.
(2018) Metals in fungal virulence. FEMS Microbiol Rev 42(1), fux050. (Review)
(2018) Power spectrum consistency among systems and transducers. Ultrasound Med Biol 44(11), 2358-2370.
(2018) Metabolic adaptation of intracellular bacteria and fungi to macrophages. Int J Med Microbiol 308(1), 215-227. (Review)
(2017) The fungal pathogen Candida glabrata does not depend on surface ferric reductases for iron acquisition. Front Microbiol 8, 1055.
(2017) Zinc limitation induces a hyper-adherent goliath phenotype in Candida albicans. Front Microbiol 8, 2238.
(2017) The Snf1-activating kinase Sak1 is a key regulator of metabolic adaptation and in vivo fitness of Candida albicans. Mol Microbiol 104(6), 989-1007.
(2017) Candida albicans Hap43 domains are required under iron starvation but not excess. Front Microbiol 8, 2388.
(2016) A novel hybrid iron regulation network combines features from pathogenic and non-pathogenic yeasts. mBio 7(5), e01782-16.
(2015) Csr1/Zap1 maintains zinc homeostasis and influences virulence in Candida dubliniensis but is not coupled to morphogenesis. Eukaryot Cell 14(7), 661-670.
(2015) Metal ions in host microbe interactions: The microbe perspective. In: Nriagu JO, Skaar EP (eds.) Trace Metals and Infectious Diseases. The MIT Press. Strüngmann Forum Reports. ISBN: 9780262029193.
(2014) Histidine degradation via an aminotransferase increases the nutritional flexibility of Candida glabrata. Eukaryot Cell 13(6), 758-765.
(2014) Metabolism in Fungal Pathogenesis. Cold Spring Harb Perspect Med 4(12),
(2014) Regulatory networks controlling nitrogen sensing and uptake in Candida albicans. PLOS One 9(3), e92734.
(2014) Immune evasion, stress resistance, and efficient nutrient acquisition are crucial for intracellular survival of Candida glabrata within macrophages. Eukaryot Cell 13(1), 170-183.
(2013) Factors supporting cysteine tolerance and sulfite production in Candida albicans. Eukaryot Cell 12(4), 604-613.
(2012) Candida albicans scavenges host zinc via Pra1 during endothelial invasion. PLOS Pathog 8(6), e1002777.
(2012) The novel Candida albicans transporter Dur31 Is a multi-stage pathogenicity factor. PLOS Pathog 8(3), e1002592.
(2012) Zinc exploitation by pathogenic fungi. PLOS Pathog 8(12), e1003034. (Review)
(2010) Regulatory network modelling of iron acquisition by a fungal pathogen in contact with epithelial cells. BMC Syst Biol 4, 148.
(2009) Candida albicans iron acquisition within the host. FEMS Yeast Res 9(7), 1000-1012.
(2008) The hyphal-associated adhesin and invasin Als3 of Candida albicans mediates iron acquisition from host ferritin. PLOS Pathog 4(11), e1000217.