UV and the microbiome

Our skin microbiome plays an essential role in our health, whether that’s through protection against invading microbes, enhancing our natural immune system or breaking down harmful products. But how does UV interact with the microbiome?

This is an emerging area where there is now growing evidence of an additional protective role for the microbiome – ultraviolet light (UV) is one of the most prominent environmental stressors that we are exposed to daily through natural light.  

The effect of UV on our skin microbiome 

UV exposure is linked to many physical changes within our skin, such as sun burn, tanning and inflammation, as well as photoaging (that is, skin ageing caused by sunlight). Exposure to the sun, for example, accounts for 80% of the visible signs of skin ageing, which includes dryness, wrinkling and solar freckles[1,2]. Cancer risk is another area linked to UV – one study showed that individuals with early signs of sun-induced wrinkling on their necks were over four times more susceptible to skin cancer[2].

A recent study[3] has now demonstrated that exposure to both UVA and UVB – the most common forms of UV – can significantly impact our delicate skin microbiota, and this disruption may be linked to some of the physical impacts of UV exposure.

Researchers observed clear increases in some bacterial groups (such as Cyanobacteria and Fusobacteria) in participants exposed to UVA and UVB, and decreases in others (such as Lactobacillaceae). Interestingly, the extent of the changes varied between individuals, showing that some were more sensitive to UV than others. No sample sites returned to the original pre-UV state during the study, indicating that the changes are long-standing for at least 24 hours.

So, this shows the sensitivity of our skin microbiota to UV, but what does this mean for our health and wellbeing?

There is now a growing bank of evidence to suggest a knock-on effect of UV-induced microbial alterations for various aspects of our health and wellbeing, such as skin condition and susceptibility to some types of disease[4]. As well as reinforcing the importance of protecting ourselves against the sun, this highlights a potential role for skin bacteria (and microbiome-boosting ingredients, such as pre- and probiotics) in mitigating and treating the effects of UV exposure.

But how would this work? Well, skin pigmentation has long been known as our primary natural defense against the sun, with melanin absorbing harmful UV and offering antioxidant properties[5]. Bacteria (along with fungi) can also produce UV-absorbing biomolecules as protection, opening up the possibility of controlling pigmentation using microbes and pre- or probiotic derivatives, while also benefitting from their antioxidant and anti-inflammatory properties[6-8].

In line with this emerging area of research, pre- and probiotics that can induce or limit the growth of certain microbes are already emerging as a potential therapeutic means to alleviate the damaging effects of UV on the skin, including photoaging, cancer and inflammatory skin disease…


Certain pre- and probiotics can prevent or reduce UV-induced increases in transepidermal water loss (TEWL; the amount of water that evaporates through skin to the external environment), hydrogen peroxide levels and protein oxidation – all of which can drive photoaging.

Probiotics such as Faecalibacterium prausnitzii[9,10] and Lactobacillus plantarum[6], for example, have been linked to reduced photoaging in humans and mice. As well as the direct exposure of our skin microbiota to UV, there is growing interest in the role of the gut microbiome in photoaging, via the gut–brain–skin axis. Oral administration of the probiotic Bifidobacterium breve in mice prevented UV-induced TEWL and suppressed UV-induced damage to the skin[11], and orally administered prebiotics such as oligosaccharides have also been shown to prevent TEWL and UV-induced skin damage[12].

Skin cancer

Research around the role of skin microbiome in the development of UV-induced skin cancers is still in its infancy, but an altered microbial landscape could play a role in cancer development. Initial reports suggest that bacterial members can – for example – alter T-cell populations, which play a defensive role against cancerous tissue formation in the skin.

One recent study has shown higher numbers of skin bacteria such as Propionibacterium and Malassezia in normal skin relative to areas with cancerous lesions[4]; and S. aureus and Chlamydophila pneumoniae have been linked to certain types of lymphoma in skin tissue[13,14]. New treatment strategies using pre- and probiotics, such as topical antibiotics that enrich certain microbes, or anti-tumour and anti-inflammatory microbes, could therefore help prevent UV-induced skin cancers.

Oral intake of probiotics such as ‘lipoteichoic acid’ from Lactobacillus rhamnosus, for example, reduced the number of UV-induced skin tumours in mice[15]. Prebiotics such as inulin have also been reported to induce Bifidobacterium bacteria[16], which can inhibit melanoma growth[17]. There is even a growing body of evidence suggesting that the skin microbiome can enhance the effectiveness of chemotherapy, radiotherapy and immunotherapy[18,19].

Inflammatory skin disease

Several skin diseases are triggered by UV[20,21].  Acne, rosacea and seborrheic dermatitis occur in UV-exposed skin, for example, but no direct effect of UV has been proven in the progression of this group of diseases. Although there is not yet any clear evidence linking UV-related skin disease to microbial composition, early indications of potential mechanisms between microbes and the response of our skin has led to research into potential microbial treatments for inflammatory diseases.

For instance, it is thought that the antimicrobial peptide ‘LL-37’, which is produced by the skin following exposure to Propionibacterium acnes and Malassezia and induced by vitamin D, could trigger inflammation in UV-exposed areas[22-24]. Prebiotics that limit the growth of such bacteria could serve as a means to reduce inflammation. Application of ‘succinic acid’, which is produced by S. epidermis, has also been shown to reduce inflammation in skin infected with P. acnes[25].

In other skin diseases, such as psoriasis and eczema, exposure to natural light or to UVA/B can help reduce disease symptoms. Here, anti-inflammatory bacteria and pre- or probiotics could be used to increase the benefit provided by the UV. Skin microbiome transplantation, for example, has successfully reduced symptoms of atopic dermatitis – a type of eczema that tends to improve following exposure to sunlight. Roseomonas mucosa, collected from healthy humans, boosted the immune system and limited the growth of the inflammatory S. aureus bacteria in an atopic dermatitis mouse model[26], and the topical application of live biotherapeutics also successfully reduced disease severity and the presence of S. aureus in patients[27].

So, although researchers are still building evidence, it seems that our skin microbiota can play a critical role in UV exposure, and that prebiotic and probiotic treatments are promising strategies to mitigate the effects of UV-induced damage.

Browse the Content Hub for more and follow us on Instagram if you are interested in reading more about current and emerging trends in the skin microbiome.


1. Grant,W.B. Eur. J. Cancer 44, 12–15 (2008).

2. Wendt, J.; Schanab, O.; Binder, M.; Pehamberger, H.; Okamoto, I. Pigment. Cell Melanoma Res. 25, 234–242 (201).
3. Burns, E. M. et al. Exp. Dermatol. 28, 136–141 (2020).

4. Patra, V. K. et al. Nutrients 12, 1795 (2020).

5. Brenner, M. & Hearing, V.J. Photochem. Photobiol. 84, 539–549 (2008).

6. Rastogi, R.P. & Incharoensakdi, A. Photochem. Photobiol. Sci.  13, 1016–1024 (2014).

7. El-Naggar, N.E. & El-Ewasy, S.M. Sci. Rep. 7, 42129 (2017).

8. Chongkae, S. et al. J. Basic Microbiol. 59, 1092–1104 (2019).

9. Heymann, W.R. J. Am. Acad. Dermatol. 53, 485–486 (2005).

10. Halder, R.M. & Bridgeman-Shah, S. Cancer 75, 667–673 (1995).

11. Slominski, A. & Paus, R. Mol. Cell Endocrinol. 99, C7–C11 (1994).

12. Hong, K.B. et al. Int. J. Food Sci. Nutr. 66, 923–930 (2015).

13. Mirvish, J.J. et al. Clin. Dermatol. 31, 423–431 (2013).

14. Nguyen, V. et al. J. Am. Acad. Dermatol. 59, 949–952 (2008).

15. Friedrich, A.D. et al. Eur. J. Immunol. 49, 2095–2102 (2019).

16. Fehlbaum, S. et al. Int. J. Mol. Sci. 19, 3097 (2018).

17. Li, Y. et al. Nat. Commun. 10, 1492 (2019).

18. Alexander, J.L. et al. Nat. Rev. Gastroenterol. Hepatol. 14, 356–365 (2017).

19. Iida, N. et al. Science 342, 967–970 (2013).

20. Jatwani, S. & Hearth Holmes, M.P. Subacute Cutaneous Lupus Erythematosus (StatPearls, 2020).

21. Patra, V. & Wolf, P. Exp. Dermatol. 25, 999–1001 (2016).

22. Salzer, S. et al. J. Dermatol. Sci. 76, 173–179 (2014).

23. Bandholtz, L. et al. Scand. J. Immunol. 63, 410–419 (2006).

24. Park, H.J. et al. J. Investig. Dermatol. 129, 843–850 (2009).

25. Wang, Y. et al. Appl. Microbiol. Biotechnol. 98, 411–424 (2014).

26. Myles, I.A. et al. JCI Insight 1, e86955 (2016).

27. Myles, I.A. et al. JCI Insight 3, e120608 (2018).

Keep exploring

You have Successfully Subscribed!