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Skin Lipid-Microbe Interplay Links Staphylococcus hominis to Barrier Control in Adult Atopic Dermatitis
Madhumita Bhattacharyya1,2, Felix Lauffer3,4, Manja Jargosch4,5
1Environmental Medicine - Institute of Environmental Medicine and Integrative Health, Faculty of Medicine, University of Augsburg and University Hospital of Augsburg, Augsburg, Germany.
Allergy
|August 28, 2025
Summary
Staphylococcus hominis influences skin barrier function in atopic dermatitis (AD) by altering lipid profiles and epidermal inflammation. This microbe is key to understanding lipid-microbe interactions in AD skin.
Area of Science:
- Microbiology
- Dermatology
- Biochemistry
Background:
- Skin surface lipids and commensal microbes are crucial for epidermal barrier function.
- The intricate interplay between skin lipids and microbes is not well understood, particularly in skin diseases like atopic dermatitis (AD).
Purpose of the Study:
- To investigate the relationship between skin lipids and microbial communities in atopic dermatitis (AD).
- To identify specific microbial species and lipid alterations associated with AD.
- To elucidate the role of identified microbes in AD pathogenesis.
Main Methods:
- High-resolution shotgun lipidomics and 16S amplicon sequencing were performed on skin tape strips from healthy and AD-affected individuals.
- Lipidomic data were integrated with microbial sequencing data to build lipid-microbe interaction networks.
- In vitro co-culture models using reconstructed human epidermis (RHE) were employed to study the effects of specific microbes and their products.
Main Results:
- Atopic dermatitis (AD) skin exhibited distinct lipid-microbe correlations compared to healthy skin, with reduced interaction diversity in lesional skin.
- Staphylococcus hominis (S. hominis) showed specific correlations with certain lipids, including negative correlation with non-hydroxy-dehydrosphingosine (NdS) 18:0;2/24:0;0 and positive correlation with diacylglycerols (DAGs).
- In vitro studies demonstrated that S. hominis, in conjunction with T cell supernatant from AD skin, reduced RHE thickness, induced spongiosis, and decreased NdS 18:0;2/24:0;0 levels. S. hominis also directly lowered NdS levels in lesional AD skin and reversed key inflammatory and metabolic gene expressions in RHE.
Conclusions:
- Staphylococcus hominis (S. hominis) emerges as a significant regulator of lipid-microbe interactions in atopic dermatitis (AD).
- S. hominis influences epidermal barrier function, inflammation, and differentiation processes in AD.
- These findings provide novel insights into the complex pathogenesis of AD and suggest potential therapeutic targets related to microbial modulation.
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