Creative Touch Permanent Makeup and Aesthetics

Your skin spans roughly 1.8 square metres and hosts hundreds of microbial species, though the populations vary dramatically by body site. Sebaceous areas like the face and upper chest favour oil-tolerant organisms. Cutibacterium and Malassezia species dominate here, as both depend on lipid-rich environments. Moist sites like armpits and feet support different communities: Corynebacterium and Staphylococcus species thrive in these conditions. Dry sites like forearms and legs host more diverse communities from all three major groups.

The numbers involved are genuinely striking. A single square centimetre of skin can support up to one million microorganisms. But the relationship isn’t simply “more microbes equals more problems.” Diversity and the ratio between species, community balance, matter far more than raw numbers.

This is the part that reframes everything. The skin microbiome isn’t just sitting there being tolerated by your immune system. It’s actively contributing to your barrier’s structure and maintenance.

The ceramide connection. Research in mouse models demonstrates that S. epidermidis secretes a sphingomyelinase enzyme that converts sphingomyelin, a host lipid, into ceramides, a process that provided a measurable additional source of these barrier-protective molecules and reduced water loss in damaged skin. ^[1] The mechanism is a genuine mutualism: the bacterium gains sphingomyelin breakdown products as a food source, and the host benefits from additional ceramide synthesis. Whether this mechanism operates at similarly significant levels in human skin awaits clinical confirmation. The primary evidence is from mouse models. But the biological rationale is sound, and the implications are worth understanding. Your own skin cells produce ceramide independently, but S. epidermidis contributes an additive source. This is not a redundant process.

It’s also worth noting that the relationship between ceramides and the microbiome works both ways. A 2026 double-blind study found that topical ceramide application not only replenished barrier lipids but also improved microbiome diversity scores, suggesting the barrier and its microbial community are in a genuinely bidirectional regulatory relationship, not simply a one-way dependency. ^[2]

The immune training role. S. epidermidis colonisation prompts keratinocytes to produce antimicrobial peptides, specifically LL-37 and defensin-β4, that function as front-line defenders against pathogenic invasion. ^[3] The mechanism is more sophisticated than simple defence, though. S. epidermidis activates Toll-like receptor 2 (TLR2) signalling pathways that produce β-defensin-3 and simultaneously induce regulatory proteins that prevent NF-κB overstimulation. ^[4] In practical terms, your commensal bacteria are teaching your immune system how to mount targeted defences without triggering the runaway inflammation that makes skin so reactive.

The lipid synthesis trigger. Cutibacterium acnes, yes, the bacterium associated with acne, plays a more complex role than its reputation suggests. Commensal C. acnes produces propionic acid from sebum fatty acids. This propionic acid has been shown in keratinocyte models to activate peroxisome proliferator-activated receptor alpha ( PPARα) receptors, stimulating production of barrier-protective lipids and proteins including filaggrin and loricrin. ^[5] The same propionic acid pathway lowers surface pH, maintaining the acidic environment that prevents Staphylococcus aureus from establishing a foothold.

C. acnes is not inherently an enemy. In balanced, open-pore sebaceous skin, it provides barrier lipid synthesis signals. It’s when follicles become obstructed, changing the local oxygen and pH environment, that the same organism contributes to inflammation. This distinction matters clinically because broad-spectrum anti-C. acnes treatments may remove a key signal in the barrier production chain, not just a skin problem.

Tight junctions. The microbiome’s influence extends to the structural connections between skin cells. Emerging research shows that microbiome composition can regulate Claudin (CLDN) protein expression, the proteins that control tight junction architecture between keratinocytes, directly governing intercellular permeability. ^[6] A change in your microbial community is a change in how tightly your cells seal together.

Dysbiosis (microbial imbalance) and barrier dysfunction don’t just co-exist. They amplify each other in a self-reinforcing loop.

In healthy skin, Staphylococcus aureus is present in very small numbers. The acidic surface pH, maintained by commensal metabolic activity, creates conditions it doesn’t tolerate well. Antimicrobial peptides produced by S. epidermidis and other commensals keep it in check. But when the barrier is disrupted by hard water, harsh cleansers, genetic filaggrin variants, or other stressors, surface pH rises. Transepidermal water loss (TEWL) increases. The habitat becomes less hospitable for acid-tolerant commensals and more permissive for S. aureus.

Once S. aureus establishes itself, the situation actively worsens. It produces virulence factors, including α-toxin and δ-toxin, that degrade the antimicrobial peptides produced by beneficial bacteria, directly eliminating the immune defences that would otherwise control it. ^{[[7], [8]]} It produces proteases that degrade filaggrin, removing the natural moisturising factor production pathway and further elevating pH. The result is a cascade: barrier disruption drives dysbiosis, dysbiosis drives further barrier disruption.

This loop is particularly well-characterised in atopic dermatitis. Lesional AD skin shows dramatically reduced microbial diversity, loss of S. epidermidis and Corynebacterium species, and S. aureus domination. Research into filaggrin gene variants confirms that filaggrin deficiency creates a lesional microbiome environment specifically enriched for S. aureus colonisation pathways. ^[9] The genetics of barrier dysfunction and the microbiology of skin disease are more intertwined than either field has historically acknowledged.

Several everyday factors can shift this balance, some of which are less obviously damaging than others.

Over-cleansing and harsh surfactants are among the most common disruptions. SLS-based cleansers and high-frequency washing reduce microbial diversity indiscriminately. They don’t selectively remove pathogens. The microbiome recovers, but repeated disruption can shift community composition over time.

Antibacterial soaps have a similar problem at larger scale. Products containing triclosan or other broad-spectrum antimicrobials eliminate commensals alongside pathogens, reducing the populations of S. epidermidis and C. acnes that are maintaining your barrier environment. There is also documented concern about antimicrobial resistance gene accumulation from long-term antibacterial product use.

Topical antibiotic overuse deserves a specific mention. Antibiotic spot treatments and long-term antibiotic topicals reduce C. acnes populations, which does address one driver of inflammatory acne, but also removes the PPARα lipid synthesis signal and contributes to the antibiotic resistance burden on skin surfaces. This isn’t an argument against antibiotics where clinically indicated, but it does suggest that indefinite long-term topical antibiotic use carries microbiome costs that warrant consideration.

Stress and cortisol operate through a more internal route. Psychological stress triggers hypothalamic-pituitary-adrenal (HPA) axis activation, releasing cortisol and catecholamines that impair keratinocyte differentiation, reduce lipid production, and increase transepidermal water loss, all of which alter the skin surface environment in ways that favour dysbiosis. ^[10] There’s evidence that this works bidirectionally: dysbiosis itself can elevate inflammatory tone, which worsens stress sensitivity. Short-chain fatty acids (SCFAs) produced by commensal bacteria may contribute to modulating neuroinflammation, connecting the skin and brain in ways that research is only beginning to characterise.

UV radiation and air pollution alter skin microbiome composition through direct and indirect mechanisms. Both UVA and UVB can promote the growth of lipophilic organisms while disrupting commensal balance. Chronic pollution exposure, particularly particulate matter and polycyclic aromatic hydrocarbons, shifts microbiome composition at the community level.

Hard water works through the pH mechanism. Elevated mineral content in hard water raises skin surface pH during cleansing, disrupting the acidic habitat that commensals depend on, and creating conditions that favour S. aureus. If you’ve encountered this in our hard water article how hard water raises skin pH, the mechanism will be familiar. The cross-article connection is worth reinforcing: what disrupts pH disrupts the microbiome, and what disrupts the microbiome disrupts the barrier.

The single most impactful daily choice for your skin’s microbial community is how you cleanse. pH-balanced, gentle cleansers, synthetic detergent (syndet) formulas in particular, cleanse without stripping the acidic surface environment that commensals require. The goal isn’t sterilisation. A clean skin surface means a surface where beneficial bacteria can maintain their populations and function, not a surface from which everything has been removed.

Frequency matters as much as product choice. Twice-daily cleansing with a gentle formula is very different from twice-daily cleansing with an SLS-based or antibacterial product.

These three categories are frequently conflated in marketing materials, and the evidence behind each is genuinely different.

Postbiotics are currently the most practically viable microbiome-targeted ingredient category in skincare. Unlike live probiotics, they don’t require bacterial viability to deliver their effects. Clinical evidence confirms they can reduce transepidermal water loss and downregulate pro-inflammatory cytokines, including TNF-α and IL-1β, and support filaggrin and involucrin expression. ^{[[11], [12]]}

A real-world example worth naming: La Roche-Posay’s reformulation of Lipikar Baume AP+M around the postbiotic Vitreoscilla filiformis lysate represents a meaningful shift in how a major skincare manufacturer thinks about barrier products. From general emollient to targeted microbiome intervention.

Live probiotic topicals are worth approaching with more caution. Without characterised strains and stability data, a product claiming “probiotic” benefits may be providing little beyond whatever else is in the formula.

Tallow’s fatty acid profile, including oleic, palmitic, and stearic acids, overlaps with the skin’s own lipid composition. A 2024 scoping review confirmed the theoretical basis for its biocompatibility with the stratum corneum. ^[13] Whether applying tallow directly supports the substrate environment for specific commensal bacteria is biologically plausible. S. epidermidis and C. acnes both depend on skin lipids as nutrients. But this mechanism has not been directly measured in published studies. Our framing is that tallow provides a sebum-compatible lipid substrate that the barrier can use, and that the microbiome’s preferred habitat, a lipid-rich, slightly acidic surface, may benefit indirectly.

Those with acne-prone skin should be aware that tallow’s saturated fatty acids can be comedogenic in susceptible individuals. Patch-testing before widespread use is sensible.

Beyond postbiotics and barrier lipids, a few other categories are worth noting. Fermented ingredients in skincare have received research interest for their prebiotic and postbiotic properties. Honey has well-documented prebiotic activity and a pH close to the skin’s optimal acidic range. And keeping ingredient lists shorter, reducing the synthetic preservative load on the skin surface, is a reasonable precaution, given that some preservatives (particularly those with broad-spectrum antimicrobial activity) may affect commensal populations at high concentrations.

The evidence is clearest here. Regular use of antibacterial soap on the face and body reduces commensal populations without meaningful benefit for most healthy adults. High-frequency use of antimicrobial actives, prescription topicals or high-strength actives used daily rather than occasionally, carries a cumulative microbiome cost. Aggressive over-exfoliation removes commensal bacteria alongside dead skin cells and disturbs the surface environment in ways that take time to restabilise.

None of this means never using these products. Weekly exfoliation is different from daily. An antibiotic course for a genuine infection is different from indefinite maintenance use. Dosage and frequency are the variables that matter.

Too often, discussion on ageing and the microbiome tends to state that the microbiome “changes with age” and leave it there. The research picture is considerably more precise.

Research presented at the 2025 Science of Skin Summit, ^[17] drawing from high-depth DNA sequencing studies comparing younger adults, community-dwelling older adults, and frail older adults, found that physiological frailty, not chronological age, drives the most significant microbiome destabilisation. Frail skin showed increased community heterogeneity, reduced microbial resilience, and the highest burden of antibiotic resistance genes on skin surfaces. Chronological age produced less stark effects. A 2025 study confirmed that ageing-dependent skin microbiome changes are site-specific. The pattern differs significantly between face, arm, and trunk sites, with loss of Cutibacterium acnes dominance on the face in older skin being a notable marker. ^[18]

In one multi-study analysis presented at the 2025 Science of Skin Summit, drawing on data from over 650 women, increased skin microbiome diversity was actually associated with more lateral canthal lines and higher transepidermal water loss. This “hyperdiversity” of ageing skin may itself be a sign of community fragility rather than richness. The commensal community becomes less organised, less dominated by beneficial keystone species.

The practical reframe: this isn’t about age being a problem. It’s about understanding that as skin physiology changes, sebum production decreases, cell turnover slows, hydration gradients shift, and the microbial community changes with it, because the habitat has changed. That’s a reason to adjust your approach, not to panic.

Oestrogen decline during perimenopause and menopause affects the skin’s microbial community through at least three parallel pathways, and it’s worth presenting all three together because the combined picture is more clinically meaningful than any single mechanism.

First: oestrogen directly supports ceramide synthesis in the skin. Its decline reduces ceramide production independent of any microbial effect. Second: oestrogen supports filaggrin expression, another direct barrier protein effect. Third, and most specific to the microbiome: a 2024 pilot study of 44 women using 16S rRNA gene sequencing found that postmenopausal skin showed significantly reduced Lactobacillus abundance compared to premenopausal skin (Pagac et al. 2024). ^[19] The researchers propose this may reflect declining oestrogen reducing glycogen availability, the substrate Lactobacillus requires for growth, though this mechanism has not yet been directly measured in skin tissue. The finding warrants further investigation.

Lactobacillus contributes to skin acidification through antimicrobial metabolite production, so its reduction may add to the pH-maintenance challenges already created by the reduced C. acnes activity seen in older, less sebaceous skin.

The combined picture: menopause doesn’t just deplete one barrier component. It simultaneously reduces ceramide synthesis, reduces filaggrin expression, and alters the microbial community that maintains the acidic surface environment. That’s a genuinely useful frame for understanding why perimenopausal skin often changes in ways that seem disproportionate to what any single skincare adjustment can address. The research group behind the Pagac study specifically proposed that microbiome-targeted interventions may offer an alternative or adjunct to HRT for managing perimenopausal skin changes, something worth tracking as the evidence develops.

Most aesthetic descriptions of cold atmospheric plasma (CAP) focus on its general antimicrobial and anti-inflammatory properties. The specific microbiome data tells a more nuanced and more interesting story.

A 2025 clinical study used next-generation sequencing to examine microbiome composition before and after plasma treatment in ten patients with acne vulgaris and atopic dermatitis. ^[20] At 24 hours post-treatment, C. acnes decreased from 31.2% to 16.2%, S. aureus decreased from 4.2% to 2.1% in AD patients, whilst S. epidermidis increased from 10.8% to 11.7% across all patients. Critically, Simpson’s Index, a measure of microbiome diversity, significantly improved (P=0.045). This is a small study, and the S. epidermidis increase is modest in absolute terms, but the diversity improvement is the more clinically meaningful headline: the microbial community became more balanced, not just smaller.

A separate prospective pilot study of 22 patients with atopic dermatitis confirmed that CAP treatment significantly reduced the S. aureus proportion in lesional skin whilst improving clinical severity scores. ^[21]

The mechanism for this selectivity is worth understanding. CAP generates reactive oxygen and nitrogen species (RONS) that are particularly effective against S. aureus and its biofilm. Cold atmospheric plasma has demonstrated significant antibiofilm activity against S. aureus, achieving multi-log reductions in viable biofilm cells in laboratory studies. This is a promising finding for skin conditions where biofilm-forming bacteria contribute to chronic inflammation. ^[22] CAP also enhances macrophage killing of S. aureus, including antibiotic-resistant MRSA strains, through oxidative mechanisms. ^[23] A 2025 Frontiers in Bioengineering study confirmed that low-temperature cold plasma promotes wound healing by improving skin microbiome composition alongside reducing inflammation. ^[24]

There’s also a third mechanism worth noting. CAP treatment has also been shown to restore tight junction integrity in keratinocytes, a finding demonstrated in a 2022 study of psoriatic skin, which may support improved intercellular sealing in barrier-damaged tissue. ^[25] This gives CAP a three-channel approach to barrier restoration: antimicrobial selectivity, immune enhancement, and structural tight junction repair.

The key distinction from antibiotics is important here. Antibiotics reduce bacterial populations broadly. CAP appears to rebalance the commensal-to-pathogen ratio, reducing the pathogens whilst the commensals recover, rather than depleting the entire community.

For clients dealing with persistent skin issues where dysbiosis may be a factor, barrier damage with bacterial involvement, reactive skin that won’t settle despite consistent home care, cold atmospheric plasma treatment is one of the few clinic-based treatments that addresses the microbial environment directly, not just the inflammation it causes. These early studies are promising, but it’s important to be clear that larger randomised trials are needed to confirm the microbiome-rebalancing effect definitively.

Blue LED light at 415–420nm targets C. acnes through a specific mechanism: porphyrins are natural metabolic byproducts of C. acnes that act as endogenous photosensitisers, and blue light activates them to create reactive oxygen species within the bacterium. ^[26] This creates a relatively selective mechanism. Blue light disrupts acne-associated C. acnes overcolonisation without the broad-spectrum bacterial destruction of antibiotic treatments.

Red LED at 630–660nm works differently. It supports keratinocyte function and barrier repair through mitochondrial stimulation, indirectly supporting the microbiome habitat by restoring the barrier conditions that commensals require.

LED therapy doesn’t fundamentally rebalance dysbiosis in the way CAP does, but it modulates the microbial environment in a condition-specific way. It’s complementary to CAP for different presentations.

A few words on timing, because this applies to any treatment plan that includes active chemical or physical interventions.

Chemical peels cause temporary broad microbiome disruption, removing a layer of skin alongside the commensal community living on it. Recovery is the period when the microbiome re-establishes, and supporting that process with gentle cleansers, postbiotic moisturisers, and avoidance of antibacterial products during recovery makes biological sense.

Retinoids alter skin cell turnover and the surface environment in ways that can affect commensal populations during the adjustment period. Using microbiome-supportive products alongside retinoid introduction, particularly postbiotic formulas, may help smooth the adaptation phase.

The pattern across all active treatments is the same: the disruption phase is temporary, but what you do during recovery influences which bacteria repopulate and in what proportions.