The Skin Microbiome
Dry, moist, and sebaceous — three ecosystems on one organ.
What's covered
- 01Skin niches: sebaceous (Cutibacterium), moist (Staphylococcus, Corynebacterium), dry (mixed)
- 02Cutibacterium acnes and acne pathogenesis
- 03Staphylococcus aureus in atopic dermatitis
- 04Malassezia and seborrheic dermatitis / dandruff
- 05Wound healing and the microbiome
- 06Microbiome-based therapeutics: bacteriotherapy for AD, acne
By the end of this module you will be able to
- L01Map the three major skin microenvironments to their dominant microbial residents.
- L02Explain the role of C. acnes strain-level diversity in acne pathogenesis.
- L03Describe how S. aureus colonization drives atopic dermatitis flares.
- L04Evaluate emerging microbiome-based skin therapeutics.
What you should walk away believing
- →Skin is three ecosystems, not one — sebaceous, moist, and dry sites host different communities.
- →C. acnes is commensal in healthy skin; specific ribotypes are acne-associated — it's strain, not species.
- →S. aureus dominance in AD is both consequence and driver of flares.
What this means for you
Your skin has different zones with different bacteria — oily areas around your nose and forehead host different microbes than your armpits or forearms. The bacterium linked to acne (C. acnes) actually lives on everyone's skin — only certain strains cause problems. Similarly, eczema flares are associated with overgrowth of Staph aureus.
Skin microbiome composition is topography-driven: sebaceous sites (Cutibacterium), moist folds (Staphylococcus, Corynebacterium), dry sites (diverse, low-biomass). In acne, strain-level (ribotype) differences in C. acnes matter more than presence/absence. In AD, S. aureus colonization correlates with flare severity and precedes flares in longitudinal studies. Topical bacteriotherapy (e.g., R. mucosa, S. hominis) is in Phase II trials.
CRISPR-based strain tracking and single-cell metagenomics are revealing that what we called 'C. acnes' is a heterogeneous clade with distinct virulence factor profiles. The antimicrobial peptide axis (LL-37, β-defensins) is a bidirectional interface — host AMPs shape the microbiome, and commensals modulate AMP expression.
Eczema and the microbiome question
Parents of a 6-year-old with moderate atopic dermatitis ask whether 'microbiome-friendly' skincare products could replace their child's topical corticosteroids. They've read about bacteria-based creams online.
How would you explain the role of S. aureus in AD, the current state of bacteriotherapy research, and the importance of not discontinuing proven treatments for unvalidated alternatives?
What the data says
Test yourself
Spaced review
Key terms & abbreviations
- Cutibacterium acnesC. acnes
- Gram-positive anaerobe dominant on sebaceous skin; strain-level variation determines pathogenicity in acne.
- Antimicrobial peptidesAMPs
- Host-produced peptides (e.g., LL-37, defensins) that shape the skin microbiome and provide innate immune defense.
Optional deeper dive
- Topographical and temporal diversity of the human skin microbiome — Grice EA & Segre JA, Science 2011↗