Exposure to UV radiation triggers a 30% shift in skin bacteria composition, weakening the usual immune tolerance to UV exposure. Digest
Ultraviolet radiation affects the skin's microbial community, influencing immune function. A recent study found that exposure to ultraviolet B radiation caused a temporary but substantial shift—roughly 30%—in the composition of skin bacteria in mice, altering the skin's response to allergens.
Using an animal model of immune suppression, researchers exposed mice to ultraviolet B radiation, collected skin samples, and assessed changes in the skin microbiome and its environment. They also used germ-free mice to isolate the effects of specific microbes and examined the role of a major photoproduct of ultraviolet radiation called cis-urocanic acid.
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They found that ultraviolet B exposure caused a rise in cis-urocanic acid, which promoted the growth of bacteria, such as Staphylococcus epidermidis, that can break it down. These bacteria used an enzyme called urocanase to metabolize the compound, lowering its levels on the skin. As a result, cis-urocanic acid lost its ability to suppress immune responses, weakening the usual tolerance that follows ultraviolet exposure. However, when the researchers applied a topical inhibitor that blocked urocanase, the bacteria could no longer break down the compound, and its immunosuppressive effects returned.
These findings suggest that specific skin bacteria can influence the immune system's response to ultraviolet radiation by degrading key photoproducts. The study investigators theorized that incorporating urocanase enzymes into sunscreen products may help maintain the skin's immunoprotective role.