Abstract

Perturbations in the skin microbiome are associated with numerous skin diseases. Three of these conditions (atopic dermatitis, acne vulgaris, and psoriasis) account for approximately half of the global burden of all skin diseases. Changes in staphylococcal communities have been linked to the severity of these diseases. No work has yet evaluated how acne therapies change the abundance of staphylococcal strains. We hypothesized that systemic acne medications like isotretinoin promote the growth of some but not all staphylococci. To test this prediction, we performed haplotype network analysis on our group’s previously published isotretinoin microbiome data set. We identified staphylococcus strains associated with distinct clinical conditions. An assessment of all available skin microbiome data sets then determined that 23 of our staphylococcus strains were present in other studies that had investigated similar but distinct conditions in other patient groups. To extend this work, we developed a skin microbe isolate collection of >500 strains, and then performed whole genome sequencing on a subset of our staphylococcus strains. This work identified enrichment of specific genes/pathways in S capitis/caprae, S epidermidis, and S warneri isolated from isotretinoin subjects. Subsequent structural analysis of the protein-encoding genes suggests that metal biology plays a role in how isotretinoin reshapes microbial communities. This investigation links established medical treatments with specific staphylococcal community perturbations, and thus provides the foundation necessary to develop precision medicine therapies to heal staphylococcal skin disease.

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