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.
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