Prof. Salomé LeibundGut-Landmann

Keywords

allergy, fungal commensals, infection, inflammation, Malassezia

What we investigate

Our laboratory studies skin commensal fungi and their role in homeostasis and disease. We are interested in the immunological mechanisms that maintain fungal commensalism on the skin, which can however also contribute to skin inflammatory and allergic conditions. We aim at understanding these processes at a cellular and molecular level.

Our research in more detail

Research Figure LeibundGut-Landmann
Commensalism: Homeostatic immune mechanisms involving IL-17 and IL-22 cytokines keep in check fungal skin commensals. Infection: Skin barrier defects and impaired immune defenses predispose to skin fungal infections. Immunopathology: Dysregulated antifungal immunity is associated with the pathogenesis of chronic inflammatory skin disorders such as psoriasis and atopic dermatitis. Our lab studies the impact of fungal determinants in the balance between these three processes.

The skin is densely colonized with microbes comprising not only bacteria but also fungi, which in the healthy skin live in equilibrium with the host. Under conditions of impaired host defences and defective skin barrier functions however, commensal fungi become associated with inflammatory and/or allergic disorders.

The causal relationship between fungal commensals and pathological skin conditions remains unclear. This important question calls for better understanding of the underlying cellular and molecular mechanisms of fungi-host interactions. An important aim of our work is to dissect how anti-fungal αβ and γδ T cells characterized by host-protective IL-17 production in the healthy skin get dysregulated and convert into pathogenic Th17 and Th2 cells in atopic individuals. A second interest of our group is devoted to the identification and characterization of fungal metabolites that can modulate tissue integrity and inflammation by engaging the host aryl hydrocarbon receptor (AhR).

We use the mouse as a model organism to address these questions. Collaboration with clinical partners will help to determine the importance of our findings for the human situation and to transfer our research results into clinical practice.

Selected publications

SKINTEGRITY.CH Principal Investigators are underlined:

  • Sparber F, De Gregorio G, Steckholzer S, Ferreira FM, Dolowschiak T, Ruchti F, Kirchner FR, Mertens S, Prinz I, Joller N, Buch T, Glatz M, Sallusto F and LeibundGut-Landmann S. 2019. The skin commensal yeast Malassezia triggers a type 17-response that coordinates anti-fungal immunity and exacerbates skin inflammation. Cell Host & Microbe. 25(3):389-403.e6. doi: 10.1016/j.chom.2019.02.002

  • Sparber F. and LeibundGut-Landmann S. 2019. Infecting Mice with Malassezia spp. to Study the Fungus-Host Interaction. J. Vis. Exp. 153:e60175. doi:10.3791/60175

  • Zwicky P., Ingelfinger F., Silva de Melo B.M., Ruchti F., Schärli S., Puertas N., Lutz M., Phan T.S., Kündig T.M., Levesque M.P., Maul J.T., Schlapbach C., LeibundGut-Landmann S., Mundt S., Becher B. 2021. IL-12 regulates type 3 immunity through interfollicular keratinocytes in psoriasiform inflammation. Sci.Imunol. 6(64): eabg9012. doi: 10.1126/sciimmunol.abg9012

  • Ianiri G., Coelho M.A., Ruchti F., Sparber F., McMahon T.J., Fu C., Bolejack M., Donovan O., Smutney H., Myler P., Dietrich F., Fox D. III, LeibundGut-Landmann S. and Heitman J. 2020. HGT in the human and skin commensal Malassezia: A bacterially derived flavohemoglobin is required for NO resistance and host interaction. PNAS. 117(27):15884. doi.org/10.1073/pnas.2003473117

  • Applen C.S.*, Ruchti F.*, LeibundGut-Landmann S., Heitman J. and Ianiri G. 2020. A Novel Mycovirus Evokes Transcriptional Rewiring in the Fungus Malassezia and Stimulates Beta Interferon Production in Macrophages. mBio. 11(5):e01534-20. doi: 10.1128/mBio.01534-20 [* equal contribution]