Characterizes facial skin microbiota in acne patients, highlighting potential therapeutic strategies.
Acne vulgaris is a chronic inflammatory disorder of the pilosebaceous unit in which skin microbiome dysbiosis plays a key pathogenic role. This study, based on full-length 16S rRNA gene amplicon sequencing (V1-V9), characterized facial microbial diversity in 45 participants classified as healthy (n=15), mild acne (n=15), and moderate-severe acne (n=15), using pooled samples for downstream microbiome analyses. Samples from the skin surface and sebaceous follicles were analyzed by 16S rRNA (V1-V9) sequencing using Illumina MiniSeq and processed via QIIME2. Alpha diversity (observed taxa, Shannon index), beta diversity (Bray-Curtis dissimilarity, permutational multivariate analysis of variance [PERMANOVA]), and biomarker taxa (linear discriminant analysis effect size [LEfSe]) were assessed. Bacillota, mainly Staphylococcus spp., predominated on the skin surface, with relative abundance increasing with acne severity, whereas follicles were dominated by Cutibacterium acnes (Actinomycetota). Follicular samples showed lower richness and Shannon diversity than surface samples, though intergroup differences were not significant. Principal coordinates analysis (PCoA) explained >65% of variation, revealing greater dispersion among surface communities but no clear clustering by severity (PERMANOVA p>0.3). LEfSe identified distinct bacterial biomarkers across clinical groups. Overall, site-specific microbial shifts - particularly C. acnes and Staphylococcus dysbiosis - appear central to acne development, suggesting microbiome-targeted interventions as potential therapeutic strategies.
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Xd et al. (2026) studied this question.
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