Key points
- In atopic dermatitis (eczema), flares track an overgrowth of Staphylococcus aureus as overall skin diversity collapses[1].
- S. aureus abundance correlates with disease severity, and barrier dysfunction and microbial overgrowth reinforce each other[1][2].
- Protective commensals fight back: certain Staphylococcus hominis and S. epidermidis strains produce antimicrobials that suppress S. aureus[3].
- Because the problem is overgrowth-plus-barrier-failure, restoring commensals and barrier matters as much as reducing the troublemaker.
Eczema is a barrier-and-community problem
Atopic dermatitis combines a leaky skin barrier, an over-reactive immune response, and a disturbed microbiome — each feeding the others[1]. A weakened barrier loses water and lets irritants and microbes in; that provokes inflammation; inflammation further degrades the barrier. The microbiome sits in the middle of this loop.
The S. aureus bloom
The signature microbial event in an eczema flare is the expansion of Staphylococcus aureus. As it blooms, the diversity of the skin community drops, and the degree of S. aureus dominance tracks how severe the flare is[1]. In infants, impaired barrier function and S. aureus colonization appear together early in life, consistent with the barrier and the microbiome co-failing rather than one simply causing the other[2].
| Staphylococcus aureus | abundance (tracks severity) |
| Overall diversity | richness of the community |
| Staphylococcus hominis / epidermidis | protective commensals |
| Barrier proteins (filaggrin, loricrin) | expression |
Direction reflects active/flaring lesional skin; the picture partly normalizes as flares resolve.
The skin’s own defense
One of the more hopeful findings is that the skin already makes its own antibiotics against S. aureus. Specific commensal strains — notably some S. hominis and S. epidermidis — secrete antimicrobial peptides that selectively suppress S. aureus, and applying these commensals has reduced S. aureus on eczema-prone skin in research settings[3]. The same commensals can nudge barrier-gene expression back up through host signalling pathways[3]. In other words, the community contains its own brake; eczema is partly the failure of that brake.
Why this reframes care
If a flare is overgrowth plus barrier failure, the logic is to reduce S. aureus while rebuilding both the commensal population and the barrier — not to sterilize the skin, which removes the protective strains too. That is the balance-restoring approach, and it is why barrier-supportive, microbiome-friendly routines are emphasized alongside flare control.
Common questions
Does Staphylococcus aureus cause eczema?
S. aureus overgrowth is a central feature of eczema flares and its abundance tracks severity, but eczema is not simply an S. aureus infection. It is a loop of barrier dysfunction, immune over-reactivity and microbial imbalance. S. aureus both worsens and is worsened by the other two — so reducing it helps, but rebuilding the barrier and the protective commensals matters just as much.
Why does my eczema skin lack “good” bacteria?
During flares, the overgrowth of S. aureus coincides with a drop in overall diversity, including protective Staphylococcus hominis and S. epidermidis strains that normally suppress S. aureus. Losing those commensals removes one of the skin’s natural brakes on the overgrowth, which is part of why flares perpetuate themselves.
Are probiotics or commensal bacteria useful for eczema?
Research is promising: specific commensal strains produce antimicrobials against S. aureus and can support barrier repair, and applying them has reduced S. aureus on eczema-prone skin in studies. This is an active area rather than a finished over-the-counter solution, and barrier care remains foundational. Discuss options with a clinician.
Should I use antibacterial washes on eczema?
Aggressive, broad antibacterial routines can reduce S. aureus but also strip the protective commensals and can further disrupt the barrier. The current direction favors gentle, barrier-supportive, microbiome-friendly care combined with targeted flare control under clinical guidance, rather than blanket sterilization.
Barrier-first, microbiome-friendly care
Eczema-prone skin needs the barrier rebuilt while the troublemaker is kept down. Parallel’s Skin Barrier Biotic™ Cream pairs prebiotics, probiotics and postbiotics with barrier-repairing ceramides and allantoin — formulated to support commensals rather than scorch them.
Explore eczema care →Cosmetic skincare offered by Parallel Health. Not intended to diagnose, treat, cure or prevent any disease; for diagnosed eczema, consult a licensed clinician.
References
- Atopic dermatitis and the skin microbiome: interplay of microbiome, barrier and immunity (review). 2024. https://pmc.ncbi.nlm.nih.gov/articles/PMC11034722/
- Berents TL, et al. Skin barrier function and Staphylococcus aureus colonization in infants with eczema: a population-based cohort study. PLoS One. 2015;10(6):e0130145. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4466520/
- Lee E, et al. Potential therapeutic skin microbiomes suppressing S. aureus-derived immune responses and upregulating barrier genes via the AhR pathway. Int J Mol Sci. 2022;23(17):9551. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9455615/