09 July 2012

The Biological Mechanism Of Sunburn

A sunburn is a condition when sunlight or ultraviolet light the skin is exposed to, exceeds the normal amount it can take and damages the exposed area. The skin has melanin which serves as the protective pigment from ultraviolet light. When there is too much ultraviolet light, the layer of skin starts to burn forming reddish skin.

Minor exposure results in a suntan although excessive amounts can be dangerous and even lethal. A serious sunburn is as serious as a thermal burn, and may have the same systemic effects such as blistering, edema and fever.

The symptoms of a sunburn are usually temporary but the damage done can be permanent and even have long term health effects such as skin cancer. Sunburn symptoms can include:
  • Red, tender skin that is warm to touch.
  • Blisters
  • Sun Poisoning that induces fever, chills, nausea, or rash
  • Skin peeling on sunburned areas

Blisters and skin peeling usually manifest itself hours or even days later.

Researchers describe inflammatory mechanism for first time

The biological mechanism of sunburn – the reddish, painful, protective immune response from ultraviolet (UV) radiation – is a consequence of RNA damage to skin cells, report researchers at the University of California, San Diego School of Medicine and elsewhere in the July 8, 2012 Advance Online Publication of Nature Medicine.

The findings open the way to perhaps eventually blocking the inflammatory process, the scientists said, and have implications for a range of medical conditions and treatments.

Video: Sun Safety

"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," said principal investigator Richard L. Gallo, MD, PhD, professor of medicine at UC San Diego School of Medicine and Veterans Affairs San Diego Healthcare System. "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."

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, neighboring cells to start a process that results in an inflammatory response intended to remove sun-damaged cells.

We see and feel the process as sunburn.

A photomicrograph of superficial keratinocytes or skin cells.
Credit: Thomas Deerinck, National Center for Microscopy and Imaging Research, UC San Diego.
"The inflammatory response is important to start the process of healing after cell death," said Gallo. "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."

Gallo said it's still not known how gender, skin pigmentation and individual genetics may affect the mechanism of sunburn. "Genetics is closely linked to the ability to defend against UV damage and develop skin cancers," he said. "We know in our mouse genetic models that specific genes will change how the mice get sunburn. Humans have similar genes, but it is not known if people have mutations in these genes that affect their sun response."


University of California - San Diego
Nature Medicine
Veterans Affairs San Diego Healthcare System
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