While summer days bring more hours of welcome daylight, longer exposure to the sun’s ultraviolet radiation (UVR) can damage the skin. Sunburn, inflammation, photoaging, skin cancer, and/or immune modulation can result. New research suggests that the skin microbiome may be a feasible target for novel strategies using probiotics and prebiotics for protection against UVR-induced skin damage.
Skin microbiome, in brief
The harsh landscape of skin — nutrient-poor and acidic —acts as a physical barrier to prevent the invasion of foreign pathogens while still providing a home to diverse commensal microbiota. The healthy human skin provides a variety of environments; some may be dry, humid, or oily, some warm or cold. Hence, the human skin harbors a multitude of diverse and complex communities of bacteria, fungi, viruses, archaea, and mites— collectively called the skin microbiome. To survive in a hostile environment, the resident microbes utilize resources present in the stratum corneum (horny outer layer), sweat (moisture secreted through pores), and sebum (oily secretion from sebaceous glands). In addition, the skin microbiome must maintain a healthy interplay with the skin’s immune system for its survival.
The skin microbiome is involved in a broad range of molecular and cellular processes within the skin and beyond which contribute to health and disease.
Ultraviolet radiation (UVR)
UVR, especially types UV-A and UV-B, can cause various local effects in the skin as well as systemic changes. Many effects are harmful such as cellular DNA damage but others are beneficial such as positive behavioral impacts as the result of endorphin production. In addition, Vitamin D3 (cholecalciferol) is mainly generated in the skin as a response to UVR. In its biologically active form, Vitamin D3 is an important nutrient for optimal health and wellbeing. A recent study shows a striking correlation between serum concentrations of 25(OH) D levels and the abundance of various microbes in the gut, suggesting an interaction between UVR exposure and the gut-skin axis.
Microbes & mechanisms of action in UVR skin effects
Melanin production and antioxidant effects
Skin pigmentation is protective against UVR. Melanin, a broad term for a group of natural pigments, absorbs as much as 50-70% of UVR and also possesses antioxidant properties.
Although darker skin has more protection from the sun’s harmful rays because it contains higher levels of melanin, people of all skin types can burn if they don’t wear sunscreen.
Specific microbial strains may produce compounds that could potentially be used to protect the skin from UVR and/or antioxidants that may improve skin health. In one example, the topical use of Lactobacillus helveticus supernatant on the skin had antioxidant effects on rodents.
Protection from photoaging
UVR exposure accounts for an estimated 80% of the visible signs of skin aging. This so-called “photoaging” is known to correlate with cancer risk. It is known that the skin microbiome is influenced by chronological and physiological skin aging. In addition to causing local (skin) changes in the microbiome, UVR can also lead to intestinal changes.
Probiotics
Many studies involving humans have supported the role of probiotics in attenuating UV-induced skin damage. Strains of probiotic bacteria including Lactobacillus johnsonii, Lactiplantibacillus plantarum, and Bifidobacterium breve have been shown to have beneficial effects on photoaging in humans or mice. A review of research testing the effects of probiotics in photoaging is available in this Table.
Prebiotics
Prebiotics such as galactooligosaccharides orally administeredhave been shownto prevent trans-epidermal water loss and prevent skin damage in hairless mice.
Anti-tumor effects of the microbiome
UVR exposure is linked with the development of different types of skin cancers including squamous cell carcinoma (SCC). SCC can develop from an actinic keratosis, which is a typical lesion of UVR- damaged skin. In recent studies, skin with lesions was observed to host different commensal strains than skin without lesions. An altered microbial landscape in cancerous skin may play a role in disease pathogenesis and/or progression.
Probiotics
In one study, oral intake of lipoteichoic acid from Lacticaseibacillus rhamnosus decreased the number of UV-induced skin tumors in hairless mice.
Prebiotics
Oral intake of prebiotics such as inulin and mucin has been reported to induce Bifidobacterium spp. and Akkermansia muciniphila which may be involved in inhibiting melanoma growth.
While these results with selected probiotics and prebiotics are promising, we should interpret them with caution and look forward to further study results.
Enhancement of the UVR-induced immune suppression
UVR has a profound effect on the skin’s immune system. The skin microbiome may have a role in UVR-induced immune suppression. For example, in a study using germ-free mice, the absence of a microbiome enhanced UVR-induced immune suppression. In contrast, mice with a microbiome showed diminished UVR-induced immune suppression.
Protection in UVR-induced skin inflammation
Inflammatory skin diseases such as systemic lupus erythematosus (SLE) and polymorphic light eruption (PLE) are linked to UVR exposures. While the mechanisms are not clear, recent research suggests that UVR-induced changes in microbial communities of the skin may be involved in their pathogenesis.
The use of topical anti-inflammatory probiotics could be beneficial.
In one study, Limosilactobacillus reuteri showed anti-inflammatory properties on reconstructed human skin models upon UVR-induced inflammation.
Takeaway
The use of probiotics and prebiotics to modulate the intestinal microbiota that support the skin immune response or the skin microbiota is promising in protecting the skin against UVR-induced skin damage. The number of human studies is, however, still limited and formulations that promote a commensal microbiome that can protect against UVR and suppress the growth of pathogens should be further explored.
In the meantime, slather on your high-SPF sunscreen this summer.
Key references
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