The Host Fungal Interfaces junior research group, led by Dr Slavena Vylkova and co‑authored by Dr Katrin Haupt, carried out its work from 1 October 2016 to 30 September 2022 within the interdisciplinary research centre Septomics at the Friedrich‑Schiller‑University Jena. Septomics links molecular biology, microbiology, infectious disease research, omics technologies, bioinformatics, laboratory medicine and intensive care, and is closely connected to the Leibniz‑Institute for Natural Product Research and Infection Biology (Hans‑Knöll‑Institute) and the University Hospital Jena. The project was funded through the German research framework of the Septomics centre and contributed to national initiatives such as the Center for Sepsis Control and Care (CSCC) and the InfectControl 2020 consortium.
The scientific aim was to dissect the pathophysiological mechanisms that enable the human pathogen Candida albicans to thrive in host environments and to cause severe infections, particularly in burn wounds and other open injuries. The group focused on how metabolic adaptation, especially the utilisation of alternative carbon sources such as carboxylic acids, amino acids and N‑acetylglucosamine, drives a shift in the local pH from acidic (pH 4) to alkaline (pH 7). This alkalinisation is mediated by the catabolism of amino acids, which releases ammonia and raises the surrounding pH, thereby promoting the transition from yeast to the more virulent hyphal form. The team demonstrated that the transcription factor Stp2, which regulates amino‑acid permeases, is essential for this process. Deletion of the STP2 gene produced a pronounced phenotype: the mutant strain failed to alkalinise its environment and could not efficiently form hyphae or robust biofilms. These findings confirm that metabolic state directly influences morphogenesis and virulence, extending earlier observations that link amino‑acid metabolism to pathogenicity.
In addition to the pH‑dependent morphogenetic switch, the group investigated the role of biofilm formation in chronic wound infections. Candida biofilms are frequently isolated from burn‑injured patients, where systemic candidiasis can reach mortality rates of up to 70 %. By analysing the composition and resilience of these biofilms, the researchers identified key metabolic pathways that support their development and resistance to antifungal agents. Preliminary data suggest that Stp2 also contributes to biofilm robustness, offering a potential target for therapeutic intervention.
The project’s results were disseminated through several peer‑reviewed publications and conference presentations, and they have informed subsequent translational studies within Septomics. By integrating metabolic, genetic, and environmental data, the Host Fungal Interfaces group has advanced the understanding of how Candida albicans adapts to host niches, how it modulates its virulence, and how these processes can be disrupted to improve patient outcomes in severe infections.
