Fungal symbiosis and pathogenicity

This research area investigates the mechanisms of fungal pathogenicity, focusing on virulence factors, immune evasion, and the transition from commensalism to infection. It integrates studies of colonization dynamics, infection progression, and antifungal resistance to identify biomarkers and targets for improved diagnostics and therapeutic strategies.

The Department Microbial Pathogenicity Mechanisms (MPM) looks at the dual use of Candida albicans commensal and pathogenicity factors. The human microbiome is a complex and dynamic network of competing and cooperating microbes that affects multiple aspects of the host's physiology and health. This includes metabolic activity of the gut microbiome, but also direct and indirect interactions between microbes and the host. However, the contribution of members of the mycobiota, like the commensal and opportunistic pathogenic fungus Candida albicans, to these activities is not well established. As a ubiquitous fungal colonizer of nearly 90% of humans, C. albicans is an important member of this intricate network. The role of C. albicans as a pathogen of humans is very well-established, but its commensal lifestyle and the effects it has on the host and members of the gut microbiome are less well studied. Recent studies have shown that the host immunity regulates the commensal stage of C. albicans and that, in turn, C. albicans commensalism affects immunity. Its morphological flexibility seems to play important roles in both pathogenicity and the establishment of gastrointestinal tract colonization. Our own unpublished research has shown that hydrolytic gene families and the C. albicans toxin candidalysin are not only critical pathogenicity factors, but also key commensal factors. In fact, it seems that the important roles of these factors in the commensal lifestyle can explain why they are evolutionarily conserved in this predominant commensal, but critical pathogenic fungus in predisposed patients.

We are looking for a postdoctoral candidate who is eager to elucidate the molecular mechanisms of these dual-use activities of C. albicans.

The Department Microbial Immunology (MI) focuses on C. albicans as both a commensal and a pathogen. While intestinal colonization with C. albicans does not lead to disease, it serves as the main source for systemic infections associated with fungal bloom in the gut. We are therefore interested in understanding the interplay between C. albicans colonization, microbiome composition and disturbances, diet, and the host immune system. The aim is to understand which fungal and environmental factors facilitate fungal colonization, how bacteria limit or promote fungal proliferation, and how the immune system responds. A second area of interest is systemic candidiasis and fungal-bacterial co-infections, which are common in clinical settings but understudied.

To this end, we use a combination of cell culture and in vivo colonization/infection models with a diverse range of state-of-the-art readout methods.

We welcome applications from excellent and enthusiastic postdoctoral researchers with a strong interest in the topics mentioned above, which can also be applied to non-albicans Candida species.