Atopic dermatitis can cause strong itchiness, but new research by Kyushu University could lead to development of drugs to finally put an end to sufferers’ urge to keep scratching their skin.
A team of researchers led by Yoshinori Fukui and Kazuhiko Yamamura of Kyushu University has identified a protein that plays a key role in producing itch-inducing cytokine interleukin 31 (IL-31).
Previous research had shown that IL-31 levels were 10 times or more higher in the blood of patients with atopic dermatitis, but the detailed mechanism of how IL-31 interacts with blood immune cells had not been known.
In the latest study, the researchers found that mice with atopic dermatitis were found to contain five to 10 times more amounts of the IL-31-producing protein, called endothelial PAS domain protein 1 (EPAS1), than those that didn’t have atopic skin inflammation.
When the researchers injected EPAS1 into healthy mice cells, they also found that the amount of IL-31 increased. On the other hand, when mice with atopic dermatitis were genetically engineered to control EPAS1, their IL-31 levels decreased.
The results led the researchers to believe that EPAS1 affects the levels of IL-31 and can be a source of itchiness.
This could lead to future development of drugs that directly target EPAS1, a potential breakthrough in treating atopic dermatitis.
The illness affects some 10 percent of the population in Japan, but treatment options have been limited. Doctors have mostly prescribed antihistamines, but they are often not effective in controlling itchiness.
“We would like to develop medicine that inhibits production of EPAS1 and present new treatment options,” Fukui said.
The study, funded by the health ministry and the Japan Agency for Medical Research and Development, was published Monday in the open-access journal Nature Communications.
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