Atopic dermatitis, also known as eczema and neurodermitis, is the most common skin disease in the world, and is present in up to 10-20% of children in the Alps. Some patients are affected more than others, and the effects on quality of life are measured using criteria ranging from rash severity and frequency of disease flareups to mental health and sleep quality. Atopic dermatitis feeds into other allergic and asthmatic disorders, and early treatment may prevent these associated conditions from developing. A wide range of factors contribute to atopic dermatitis, including mechanical damage to the skin, bacterial infection, and immune dysregulation. Unfortunately, existing laboratory models do not recapitulate well all 3 of these variables. Establishing a more biologically accurate model of atopic dermatitis would enable faster drug screening and wider-reaching explorations into disease development and physiology. To this end, we received skin donated by healthy patients undergoing surgery, and tested means of mechanical disruption, immune modulators, and bacterial strains isolated from the skin of atopic dermatitis patients for their ability to induce atopic dermatitis-like phenotypes in the healthy skin. Some approaches yield a robust immune response which we have characterized primarily with mass spectrometry-based proteomics of specific cell types and tissue layers. This immune response is attenuated with existing therapeutics, demonstrating that our model captures the known mechanisms of the disease. Our approach has many advantages over other models, including preservation of the organ-level structure and cellular diversity of real skin, unbiased characterization using DIA proteomics, ease of handling, and speed. Additionally, the diverse readouts also include histological and microbiological methods, enabling a comprehensive overview of disease status through various biological lenses.
