Sunburned skin is detected through release of damaged RNA, which stimulates an inflammatory response from the surrounding cells, according to research published online July 8 in Nature Medicine.
Jamie J. Bernard, Ph.D., from the University of California San Diego, and colleagues treated skin cells with acute ultraviolet B radiation to investigate how skin detects damaging levels of ultraviolet radiation that trigger the inflammatory response.
The researchers found that radiation caused release of RNA from the irradiated cells. Sequencing revealed that irradiation of keratinocytes induced alterations in some double-stranded noncoding domains. These damaged self-RNAs induced production of the inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-6 from surrounding cells. Ultraviolet-damaged self-RNAs were sufficient to induce cytokine production from nonirradiated cells, and this response was dependent on TLR3 and TRIF. Mice lacking TLR3 were unable to respond to ultraviolet radiation by producing TNF-α and unable to suppress contact hypersensitivity.
"Diseases like psoriasis are treated by ultraviolet light, but a big side effect is that this treatment increases the risk of skin cancer," a coauthor said in a statement. "Our discovery suggests a way to get the beneficial effects of ultraviolet therapy without actually exposing our patients to the harmful ultraviolet light."
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For more information on UV light exposure, read the article "The Influence of Ethnicity, Gender, and Fitzpatrick Skin Type on High School Students' Ultraviolet Light Risk Awareness and Behavior."