Consequences of Malassezia colonization on skin homeostasis

Malassezia is associated with severe and chronic inflammatory skin conditions such as atopic dermatitis (eczema). The causal relationship between the skin commensal and disease is however unclear. In this project we are interested in dissecting the mutual crosstalk between Malassezia and the host in healthy and inflamed skin to understand how Malassezia can exert host-beneficial and/or host-adverse effects in a context-dependent manner.

First, we aim at understanding how in barrier-impaired skin, such as it is typical for atopic dermatitis patients, the normally protective antifungal response mediates pathology and contributes to disease exacerbation.

Second, we investigate how Malassezia adapts to the dysfunctional epidermal barrier environment that is typical for atopic dermatitis. By increasing the expression of proteases (e.g. Sap1) it contributes to barrier impairment and inflammation, which in turn provides increased accessibility to altered lipid sources, to which the lipid-dependent yeast adapts for enhanced nutrient assimilation.

Third, we investigate how the aryl hydrocarbon receptor (AhR) in keratinocytes responds to fungal metabolites to modulates the skin barrier integrity and restore tissue homeostasis.