National Geographic News
A swimmer with a sunburn.

Sun exposure may set off chemical "alarms" in our cells, triggering inflammation.

Photograph by Jason Edwards, National Geographic

Christine Dell'Amore

National Geographic News

Published July 11, 2012

For the first time, science has illuminated why our skin reddens and stings when we get too much sunshine, a new study says.

(See more health news.)

Though "sunburn is a common experience for human beings, there's surprisingly little information on how energy in sunlight is detected [in the body] as a source of danger," said study leader Richard L. Gallo, professor of medicine and chief of dermatology at the University of California, San Diego, School of Medicine.

Now Gallo's team has identified the chemical culprit that triggers our skin's warning signs. A type of RNA, they found, breaks into pieces within a dead cell done in by ultraviolet sunlight.

Next, so-called receptor molecules in neighboring cells detects the damaged RNA and "tell" the body to inflame the healthy skin around the dead cell—and voilà: sunburn.

Usually, RNA acts as a messenger in our bodies, "coding" DNA, with which RNA shares its double-helix structure. But the kind of RNA that triggers sunburn is called noncoding RNA—it doesn't transmit genetic information, but instead controls how our genes work.

(Get a genetics overview.)

Sunburn-Triggering Molecule Does "Double Duty"

To identify sunburn's trigger, Gallo and colleagues gave human skin cells in the lab a dose of ultraviolet light equivalent to about 15 to 30 minutes in the bright sun—enough for a sunburn.

The researchers then added the dead cells to a culture of normal cells. (Read "Unmasking Skin" in National Geographic magazine.)

To the team's surprise, a type of receptor that normally detects foreign RNA in viruses also recognizes the broken RNA within the dead cells and triggers the inflammation process. "Turns out this receptor does double duty," Gallo said.

To further test this hypothesis, the scientists used genetically engineered mice that lack the RNA-detecting receptor. Then the team exposed the rodents to ultraviolet light.

The mice got fewer sunburns—suggesting that the receptor is responsible for activating inflammation in the body.

Inflammation May Actually Help

Inflammation can be beneficial for several reasons, Gallo noted. For starters, it removes sun-zapped cells, allowing the skin to heal.

The team also suspects the inflammatory process may clear out cells with genetic damage before they can become cancerous.

And, of course, sunburn is unpleasant—the inflammation "teaches us that getting that sunlight is not such a good thing," said Gallo, whose study was published July 8 by the journal Nature Medicine.

The discovery may be good for more than just summer trivia.

For example, Gallo said, by understanding how sunburn happens may help scientists develop inflammation blockers. That might be bad for most of us, but for many people with autoimmune diseases such as lupus—which can result in high sun sensitivity—thwarting inflammation would be very helpful, he said.



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