The fungus Candida albicans is a commensal microorganism in humans mainly associated with mucosal surfaces, i.e. the oral cavity, the gastrointestinal and the urogenital tract, and the skin. Under certain circumstances, such as immune suppression or disruptions of the associated microbiota, it can become pathogenic and cause a range of infections: from mild inflammation of the skin or mucosal surfaces to severe invasive infections and sepsis.

In order to survive and proliferate in the human host, this opportunistic fungal pathogen has acquired a remarkable repertoire of adaptation strategies to circumvent the host immune response and to cope with the limited nutrient supply and environmental alterations of pH, oxygen and osmolarity. Importantly, the tight association with humans, both as a commensal and a pathogen, has driven the evolution of mechanisms that permit rapid metabolic adaptations to the changing environments within the host, where the availability of nutrients is often limited. Previous work by our lab and others shows in fact that such metabolic plasticity plays an important role in pathogenicity. Therefore, we investigate the mechanistic links that connect metabolic adaptations and alterations to the commensal-to-pathogen shift, stress resistance, expression of virulence determinants, and drug susceptibility.

Adequate nutrition is a fundamental prerequisite for C. albicans persistence in the human host. The adaptation to and proliferation in nutrient-restrictive host niches is not only critical for survival, but also for the ability of the fungus to cause infection. Thus, C. albicans has evolved remarkable metabolic plasticity, such as the ability to utilize simultaneously preferred and non-preferred carbon sources or quickly switch from growth on one nutrient to another.  We are particularly interested in i) molecular mechanisms of metabolic adaptation of C. albicans and ii) the metabolic changes that accompany the transition from a commensal to a pathogen.

Candida albicans is the most common cause of mucosal and systemic candidiasis. Other related Candida species, such as Candida glabrata, Candida parapsilosis, Candida tropicalis and the emerging pathogen Candida auris have also been associated with most forms of candidiasis, though far less frequently. C. albicans is very closely related to Candida dubliniensis, with which it shares many phenotypic properties, including the ability to produce hyphae, an important pathogenicity trait. Surprisingly, despite the close phylogenetic relationship of the two species epidemiological data show that C. albicans is far more prevalently associated with the host than C. dubliniensis. Certain features, such as differences in posttranslational regulation of hyphal growth distinguish the two species. Interestingly, C. dubliniensis seems to lack the metabolic flexibility of C. albicans, but the reasons for this remain unexplored. We argue that C. albicans possess specific metabolic features lacking in the closely related C. dubliniensis and C. africana that make it both a successful colonizer and a pathogen.