When discussing the harmful effects of ultraviolet radiation on the skin, the classic picture comes to mind: DNA damage, oxidative stress, inflammation, and photoaging. These processes are well established and occur directly within skin cells — keratinocytes, fibroblasts, and melanocytes. Yet UV radiation has another target that has received far less attention: the skin microbiome — a community of billions of microorganisms inhabiting the skin surface and actively contributing to its barrier function, immune balance, and homeostasis.

It has long been known that UV radiation can alter the composition of the skin microbiome — its species diversity and the abundance of individual populations. However, the question of how exactly the chemical language through which microorganisms "communicate" with the skin changes after irradiation had remained virtually unexplored. A new study published in 2026 in Applied and Environmental Microbiology represents the first systematic step in this direction [1].

What was studied and how

A team of British researchers led by Steven Mercer at the University of Manchester selected 11 species of skin commensal bacteria representative of healthy human skin: Staphylococcus hominis, S. epidermidis, S. capitis, S. warneri, S. lugdunensis, S. aureus, Micrococcus luteus, Kocuria rhizophila, K. marina, K. palustris, and Brachybacterium rhamnosum. Each species was cultured and then exposed to solar-simulated radiation (SSR) — a laboratory analog of the full solar spectrum, encompassing both UVA and UVB components — at doses of 37.5 and 150 mJ/cm². This range corresponds to realistic everyday sun exposure.

After irradiation, the bacterial metabolome was analyzed using two mass spectrometry approaches. The first — targeted liquid chromatography–mass spectrometry (LC-MS) — enables precise identification and quantification of a predefined set of compounds in a liquid sample; in this study, it was used to measure metabolites of the specific tryptophan pathway. The second — untargeted gas chromatography–mass spectrometry (GC-MS) — is a broader exploratory approach that captures the overall metabolic "fingerprint" of a sample, allowing changes in a large number of primary metabolites — amino acids, organic acids, and other low-molecular-weight compounds — to be detected without predefined targets.

To assess the biological effect of bacterial metabolic products on skin cells, the researchers worked not with live bacteria but with their cell-free supernatants (CFSNs): the liquid medium in which bacteria had grown, cleared of the microorganisms themselves by centrifugation. In essence, CFSNs represent the "molecular message" of the bacteria — a concentrate of all the substances they secrete into their environment. CFSNs from both irradiated and non-irradiated bacteria were added to keratinocyte cultures to assess their effect on aryl hydrocarbon receptor (AhR) activation using a luciferase reporter assay, and on epidermal barrier function by measuring transepithelial electrical resistance (TEER) — an indicator of tight junction integrity and, therefore, epidermal barrier coherence [1].

The AhR is an intracellular ligand-activated receptor that, upon binding specific molecules, translocates to the nucleus and acts as a transcription factor, switching target genes on and off. Its defining feature is a remarkably broad ligand repertoire: it responds to structurally diverse molecules ranging from industrial toxicants (dioxins) to natural compounds of plant and microbial origin. In the skin, AhR is expressed primarily in keratinocytes and regulates key processes: epidermal differentiation, synthesis of structural proteins of the stratum corneum, barrier function, and local immune responses [2, 3].

Tryptophan derivatives — including those of microbial origin — are among the physiological ligands of AhR. In other words, skin microbiome bacteria normally "communicate" with keratinocytes in part through this receptor, supplying it with signaling molecules [4]. This is precisely why AhR became a central focus of the study: if solar radiation alters the spectrum of tryptophan metabolites produced by commensals, it follows that the signal the microbiome sends to the skin via AhR would also change — and with it, the keratinocyte response.

Key findings: the metabolome shifts — and not by chance

The principal finding of the study: solar-simulated radiation significantly and reproducibly alters the metabolic profile of skin bacteria, with the pattern of changes depending on both the species and the radiation dose.

At the low dose (37.5 mJ/cm²), the majority of species showed increased production of tryptophan pathway metabolites. Specifically in S. hominis, upregulated expression of the genes ipdC, ALDH, and trpE — encoding key enzymes in this pathway — was observed. This points to an active, regulated metabolic reprogramming rather than a nonspecific stress response. At the high dose (150 mJ/cm²), the picture generally reversed: production of most metabolites declined, likely reflecting more pronounced cellular damage.

Among the metabolites that changed most significantly were tryptophan derivatives: indole-3-acetamide, indole-3-acetate, indole-3-carboxaldehyde, indole-3-lactate, indole-3-acetaldehyde, tryptophol, kynurenine, and tryptamine. These compounds are well established as biologically active molecules capable of interacting with skin cells through several receptor systems — most notably AhR [1].

An altered metabolome — an altered signal

Following irradiation, CFSNs from the majority of bacteria studied — 8 out of 11 species — demonstrated significantly greater capacity to activate AhR compared to unirradiated controls. Receptor activation correlated statistically with elevated levels of indole-3-acetamide, tryptophol, indole-3-carboxaldehyde, and tryptamine.

AhR is a ligand-activated transcription factor expressed in keratinocytes, among other cell types. It is involved in regulating epidermal differentiation, synthesis of stratum corneum structural proteins, and cutaneous immune responses [2, 3]. Under normal conditions, microbial tryptophan derivatives are among the physiological sources of AhR activation, contributing to epidermal barrier maintenance and an anti-inflammatory tone [4]. Thus, UV-driven shifts in these metabolites potentially alter both the nature and intensity of this signaling.

This was most clearly demonstrated in the barrier function experiments. Keratinocytes incubated with CFSNs from irradiated M. luteus, S. hominis, and S. capitis showed significantly higher TEER values compared to unirradiated controls — indicating enhanced barrier function. However, this effect was completely abolished by the addition of the AhR antagonist CH-223191. This provides direct evidence that AhR mediates the impact of the altered microbial metabolome on the epidermal barrier [1].

An important note: the toxicity of CFSNs obtained from irradiated bacteria did not increase; keratinocyte viability following 24 hours of exposure remained comparable to unirradiated controls. This indicates that the observed effects are attributable to changes in microbial metabolite composition rather than the accumulation of toxic photolysis products.

Limitations

The authors themselves acknowledge that the specific molecules responsible for each observed effect have not yet been identified with sufficient precision. All experiments were conducted in vitro — using isolated bacterial cultures and keratinocyte monolayers — which does not replicate the full complexity of microbiome–skin interactions in living tissue. Further in vivo studies and experiments using more sophisticated models are needed to understand how these mechanisms operate under real-world sun exposure conditions.

Practical implications and conclusion

This study offers skincare specialists and dermatologists a fundamentally new perspective on the role of sunscreens. Until now, the rationale for their use rested on direct protection of skin cells from the mutagenic and photoaging effects of ultraviolet radiation. A new argument can now be added: UV filters, by reducing the intensity of solar exposure, simultaneously limit radiation-induced shifts in commensal bacterial metabolism.

If SSR-driven changes in the metabolome genuinely alter how the microbiome interacts with the skin — including through AhR-dependent barrier-maintenance mechanisms — then consistent photoprotection takes on an additional dimension: preserving the normal "dialogue" between the microbiome and the epidermis. This chain — solar radiation → commensal metabolome → AhR signaling → barrier function — has been described for the first time and opens a new chapter in the study of skin photobiology.

For now, these are preliminary fundamental findings, and it is too early to draw specific clinical recommendations. Nevertheless, the data already provide a new rationale for conversations with patients about the importance of daily, consistent photoprotection: SPF is not only about protecting keratinocytes and fibroblasts — it is also about maintaining the healthy relationship between the skin and its microbial community.

References

1. Mercer S.D., Elias A., Taylor G. et al. Ultraviolet radiation reshapes the metabolome of skin commensal bacteria, influencing AhR signaling and barrier function. Appl Environ Microbiol 2026; 92(4): 1–15.
2. van den Bogaard E.H., Bergboer J., GM., Vonk-Bergers M. et al. Coal tar induces AHR-dependent skin barrier repair in atopic dermatitis. J Clin Invest 2013;123(2): 917–927.
3. Wang X., Guo R., Qin Z. et al. Aryl hydrocarbon receptor activation promotes CXCL5-mediated neutrophil infiltration in psoriatic skin. J Invest Dermatol 2024; 144(3): 509–519.
4. Uberoi A., McCready-Vangi A., Grice E.A. The wound microbiota: microbial mechanisms of barrier function disruption and infection. Cell Chem Biol 2025; 32: 111–125.
5. Patra V., Wagner K., Arulampalam V., Wolf P. Skin microbiome modulates the effect of ultraviolet radiation on cellular response and immune function. iScience 2019;15: 211–222.