The mammalian skin is densely populated with microbes including the yeast Malassezia, which is the single most abundant fungal species on most parts of the skin. The constant exposure of the host to microbes shapes the immune system and instructs its reactivity towards insults with pathogens. Changes in the balance between the host and the microbiota can have detrimental effects for the host resulting in dysbiosis and conversion of (at least some) commensals into pathogens. Increasing evidence suggests that Malassezia is involved in the pathogenesis of a variety of common inflammatory skin diseases such as atopic dermatitis. The association of Malassezia with atopic dermatitis is based on the observation that approximately 80% of human atopic dermatitis patients show IgE-mediated sensitization and positive skin prick tests for Malassezia. However, the causal relationship between Malassezia and atopic dermatitis remains to be elucidated. Using a newly established infection model, this project will dissect the complex interplay between Malassezia and the skin immune system and decipher the protective host mechanisms that prevent fungal overgrowth in the skin. Moreover, it will explore the role of Malassezia in the manifestation of inflammatory skin diseases. This shall help to resolve the medical conundrum how Malassezia on the one hand lives as a commensal on healthy skin with putative host-beneficial effects during homeostasis, and on the other hand contributes to the pathogenesis of atopic dermatitis in patients.
Funding: Institutional funding
Malassezia furfur grown on Dixon medium