Skin Lipid-Microbe Interplay Links Staphylococcus hominis to Barrier Control in Adult Atopic Dermatitis.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 40874637.
- Also identified by DOI 10.1111/all.70028 and PMC identifier 12862556.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Skin surface lipids and commensal microbes are essential for the epidermal barrier, but their mutual interactions remain poorly understood. We conducted high-resolution shotgun lipidomics of tape strips from lesional and non-lesional atopic dermatitis (AD) skin and healthy controls. Lipidomic data were integrated with 16S amplicon sequencing to construct lipid-microbe interaction networks. AD skin showed disease-specific lipid-microbe correlations, with less diverse interactions in lesional compared to non-lesional and healthy skin. Staphylococcus hominis (S. hominis) negatively correlated with non-hydroxy-dehydrosphingosine (NdS) 18:0;2/24:0;0 and positively with diacylglycerol (DAG) 18:1;0_18:1;0 and DAG 16:0;0_18:1;0. In vitro co-cultures of reconstructed human epidermis (RHE) with AD skin-derived T cell supernatant (TCS) and S. hominis reduced RHE thickness, spongiosis, and NdS 18:0;2/24:0;0 levels. Furthermore, S. hominis directly lowered NdS 18:0;2/24:0;0 levels in lesional AD skin tape samples, and reversed type 2 inflammation and lipid metabolism gene expression in TCS-stimulated RHE. These findings identify S. hominis as a key regulator of lipid-microbe interactions in AD, influencing epidermal inflammation and differentiation.
Medical subject headings
- Dermatitis, Atopic
- Skin
- Lipid Metabolism
- Lipids
- Microbiota