Sunburn May Lead To New Drug Treatment For Chronic Pain
A molecule found in the body that controls sensitivity to pain from UVB irradiation, or sunburn, may help scientists develop new drugs to treat chronic pain conditions such as arthritis, according to a study published in the journal Science Translational Medicine.
Chronic pain is estimated to costs about $290 billion a year in Europe and about $150 billion a year in the United States, reports Reuters.
A survey conducted by a group called Pain in Europe estimates that one in every five Europeans suffer from chronic pain; and studies have shown that about 22 percent of chronic pain sufferers become depressed and a quarter of them end up losing their jobs.
Researchers discovered that the CXCL5 molecule, which is part of a family of proteins called chemokines that recruits inflammatory immune cells to injured tissue, triggers pain and tenderness.
“We’ve identified this chemokine as an important factor that drives some forms of pain, and we did that in the context of UVB irradiation or sunburn,” says Stephen McMahon from the Wolfson Center for age-related diseases at King’s College London and head of a research group called the London Pain Consortium.
“But this study isn’t just about sunburn,” he says in a phone interview with Reuters reporter Kate Kelland.
The outer layer of skin known as the epidermis is typically affected by UVB radiation, which is the primary agent responsible for sunburn.
McMahon continues: “More broadly we have identified a mediator that may be important in a variety of different pains states ““ particularly those associated with inflammation ““ and there are lots of those out there, for example in arthritis.”
Healthy volunteers were recruited for the study. Patches of their skin were exposed to UVB radiation to create small areas of sunburn.
Over the next few hours, the affected skin became tender, and pain grew to a peak about one to two days later. At its peak, researchers performed small biopsies of the affected skin and analyzed the tissue for hundreds of pain mediators.
High levels of several of these mediators were found, which included CXCL5. Armed with this information, the researchers then examined the biology of these factors in rats to determine whether the mediators were responsible for causing the pain in sunburnt skin.
Results from the study showed that CXCL5 was present at high levels in both human biopsies and the biology of the chemokine protein rats, which suggests that CXCL5 was indeed responsible for a significant amount of sunburn pain.
A neutralizing antibody that targeted CXCL5 was shown to reduce the sensitivity to pain caused by the UVB irradiation in further tests on the rats.
The next step in the study would be to develop a human version of the antibody to test in clinical trials, says McMahon.
“Giving an antibody is quite an attractive treatment strategy, because even though you have to inject it”¦ the antibody then often hangs around for weeks, and it almost totally blocks the availability of the factors it binds to,” he explains.
Reuters reports that drug makers Pfizer, AstraZeneca and GlaxoSmithKline all have drug research programs currently looking at chemokine and that McMahon says that candidate compounds were likely and could be tested in human trials very soon.
“I’m excited about where these findings could take us in terms of eventually developing a new type of analgesic for people who suffer from chronic pain.”
On the Net: