The biological mechanism of sunburn - the reddish, painful, protective immune response from ultraviolet (UV) radiation - is a consequence of RNA damage to skin cells, a new study has found.
The findings, by researchers at the University of California, San Diego School of Medicine and elsewhere, open the way to perhaps eventually blocking the inflammatory process, the scientists said, and have implications for a range of medical conditions and treatments.
"For example, diseases like psoriasis are treated by UV light, but a big side effect is that this treatment increases the risk of skin cancer,” Richard L. Gallo, principal investigator of the study, said.
"Our discovery suggests a way to get the beneficial effects of UV therapy without actually exposing our patients to the harmful UV light. Also, some people have excess sensitivity to UV light, patients with lupus, for example. We are exploring if we can help them by blocking the pathway we discovered,” he said.
Using both human skin cells and a mouse model, Gallo, first author Jamie J. Bernard, a post-doctoral researcher, and colleagues found that UVB radiation fractures and tangles elements of non-coding micro-RNA - a special type of RNA inside the cell that does not directly make proteins. Irradiated cells release this altered RNA, provoking healthy, neighbouring cells to start a process that results in an inflammatory response intended to remove sun-damaged cells.
"The inflammatory response is important to start the process of healing after cell death,” Gallo said.
"We also believe the inflammatory process may clean up cells with genetic damage before they can become cancer. Of course, this process is imperfect and with more UV exposure, there is more chance of cells becoming cancerous,” he added.
The study has been published in the Advance Online Publication of Nature Medicine.
