Ah, it's summer again. You're laying on your patio and fall asleep with a martini on the Ikea mini-table beside you. You doze off, dreaming about that Europe backpacking trip that you had planned with your best friend. Suddenly, you wake up and what's this? Your face hurts! Oh darn, you forgot to put on sunscreen and now your face is burning!
Many of us aren't strangers to sunburns. The characteristic red burning sensation when we've overstayed our time in the sun is a type of inflammation. Inflammation is a component of the many responses to harmful agents, including germs as well as damaged cells. Typically, the process involves the recruitment of immune cells, which destroy damaged tissue as well as germs, in an effort to promote healing. During inflammation, our pain-receptors become sensitized due to chemicals that are released from the white blood cells. Sunlight contains harmful ultraviolet B (UVB) rays, which promotes hypersensitivity to pain 24-48 hrs after exposure. In addition, UVB can cause dangerous mutations in your DNA leading to skin cancer, which is why sunscreen is very important.
John Dawes of Stephen McMahon's lab decided to study this inflammation response towards UVB. After exposing human and rat skin to UVB rays, they found both increased blood flow to the skin as well as the subject's pain thresholds dropping substantially. An analysis of genes that were turned on after UVB irradiation revealed that humans and mice share a similar response towards UVB damage. In addition, the gene that changed the most was a poorly-studied chemokine (chemicals that modulate the immune system) called CXCL5.
CXCL5 has previously been linked with certain chronic pain syndromes, so it looked like an interesting gene. They injected the CXCL5 protein directly into rat feet and saw that they were more susceptible to pain. In addition, they found that CXCL5 could attract white blood cells towards it, similar to a magnet pulling on metal. The cool thing was that blocking the action of CXCL5 raised the pain threshold after UVB treatment, so rats felt less pain in an artificial sunburn. In addition, there was less white blood cells being attracted to the site of injury.
Altogether, this study has found an interesting gene CXCL5 that is associated with the pain in sunburns. Drug companies are now considering developing a sunburn pain remedy that would contain a drug that specifically blocks CXCL5. However, one caveat is that less white blood cells will be attracted to the sunburn site, so one might get delayed healing of the damaged skin.
Dawes, J., et al. (2011) CXCL5 Mediates UVB Irradiation–Induced Pain. Science Translational Medicine 3(90):90ra60. Paper.
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