From commensalism to pathogenesis
The gut is believed to be the main reservoir of Candida albicans, where the fungus lives as a harmless commensal, in a peaceful cohabitation with “the good” bacteria. However, C. albicans can invade this tissue and enter the bloodstream (translocation) due to alterations of the gut’s physiology. A major risk factor is the use of antibiotics. In fact, it has been shown that the removal of protective bacteria from the gut is a prerequisite for the translocation of the fungus into the bloodstream. From here, the fungus can infect almost all organs and finally cause sepsis. Our aim is to elucidate which factors (of the fungus as well as of the host) are responsible for the shift of C. albicans to a pathogenic state.
We are using genome-wide transcription profiling techniques on in vitro (translocation and damage of host cells), ex vivo (perfused gut) and in vivo (mouse) infection models for translocation. Genes associated with colonization or translocation will be analyzed in detail with a focus on those with previously unknown function.
Another aspect which will be studied in detail is the shift from commensalism to a pathogenic state, by establishing a commensal gut model, where C. albicans grows in equilibrium with protective probiotic bacteria on intestinal epithelial tissue.
(2019) Human anti-fungal Th17 immunity and pathology rely on cross-reactivity against Candida albicans. Cell 176(6), 1340-1355.e15.
(2019) CARD9+ microglia promote antifungal immunity via IL-1β- and CXCL1-mediated neutrophil recruitment. Nat Immunol 20(5), 559-570.
(2018) Candida albicans-induced epithelial damage mediates translocation through intestinal barriers. mBio 9(3), e00915-18.
(2018) Two's company: studying interspecies relationships with dual RNA-seq. Curr Opin Microbiol 42, 7-12. (Review)
(2017) Encapsulation of antifungals in micelles protects Candida albicans during gall-bladder infection. Front Microbiol 8, 117.
(2017) Fungi that infect humans. Microbiol Spectr 5(3), FUNK-0014-2016. (Review)
(2017) Antifungal defense of probiotic Lactobacillus rhamnosus GG is mediated by blocking adhesion and nutrient depletion. PLOS ONE 12(10), e0184438.
(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.
(2016) Enemies and brothers in arms: Candida albicans and gram-positive bacteria. Cell Microbiol 18(12), 1709-1715. (Review)
(2016) Dual-species transcriptional profiling during systemic candidiasis reveals organ-specific host-pathogen interactions. Sci Rep 6, 36055.
(2016) Effects of the glucocorticoid betamethasone on the interaction of Candida albicans with human epithelial cells. Microbiology 162(12), 2116-2125.
(2014) From commensal to pathogen: Candida albicans. In: Esser K, Kurzai O (eds.) The Mycota Ed. 2. Vol. XII, pp. 3-18. Springer Verlag.
(2012) Importance of the Candida albicans cell wall during commensalism and infection. Curr Opin Microbiol 15(4), 406-412. (Review)
(2012) Candida albicans-epithelial interactions: dissecting the roles of active penetration, induced endocytosis and host factors on the infection process. PLOS One 7(5), e36952.
(2010) Cellular interactions of Candida albicans with human oral epithelial cells and enterocytes. Cell Microbiol 12(2), 248-271.
(2009) Identifying infection-associated genes of Candida albicans in the postgenomic era. FEMS Yeast Res 9(5), 688-700. (Review)
(2004) From commensal to pathogen: stage- and tissue-specific gene expression of Candida albicans. Curr Opin Microbiol 7(4), 336-341. (Review)
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