Researchers have identified the “first responders” that set off the cycle of itching and scratching in atopic dermatitis.
For the 10 percent of people who have ever experienced the dry, itchy skin and rashes of a type of eczema called atopic dermatitis, relief from this chronic condition is long overdue.
Researchers at the University of California, Berkeley have developed a new understanding of how the nervous and immune systems interact to cause the itching and inflammation typical of atopic dermatitis, which could one day lead to new therapies.
Atopic dermatitis, or allergic eczema, which affects around 10 percent of children and two percent of adults in the U.S., involves changes to the skin’s normal mechanisms of inflammation.
In people with atopic dermatitis, when the skin becomes irritated—by chemicals, allergens, or other irritants—a cycle of itching and scratching occurs that causes cracked or scaly skin. In severe cases, scratching may also lead to skin infections that require treatment with antibiotics.
There’s currently no cure for atopic dermatitis. Most treatments attempt to reduce inflammation, relieve itching, or prevent flare-ups. These include over-the-counter anti-itch creams and antihistamines like Benadryl.
To date, most of the research on atopic dermatitis has focused on identifying the chemicals that cause the itching and inflammation. Drugs in development are aimed at blocking the response of the immune system to damaged skin cells caused by repeated scratching.
“Most drug development has focused on trying to find a way to inhibit the immune response,” says UC Berkeley neuroscientist Diana Bautista, Ph.D., in a press release. “Now that we have found that sensory neurons may be the first responders, that changes how we think about the disease.”
Blocking these nerves would stop the itching before it even began. This would prevent people from scratching, which damages the skin and leads to more inflammation.
It might also head off the immune system response that can result in other allergic reactions in people with atopic dermatitis. This “atopic march,” as it’s called, can lead to food allergies, asthma, and nasal allergies.
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Currently, there are no drugs that are approved to block these sensory nerves in the skin, but the researchers have identified a potential medicine that’s currently being tested for another inflammatory disease. This topical drug has been shown to stop mice from scratching.
The skin’s reaction to irritants hinges on a cytokine known as thymic stromal lymphopoietin (TSLP). This chemical, which is released by skin cells, acts on sensory nerves and immune cells—both of which are involved in causing the symptoms of atopic dermatitis.
Researchers once thought that sensory nerves wouldn’t react unless the immune cells were first triggered by TSLP. The current study, though, showed that this is not the case.
Bautista and her colleagues have identified two possible ways to prevent sensory nerves from reacting to skin irritants. One is to block part of the receptor on the nerve that responds to TSLP, which is known as the wasabi ion channel because it responds to “mustard compounds” like those found in wasabi.
The other option would be to block the release of TSLP from damaged skin cells. Both would be potential targets for new drugs—which have yet to be developed.
One of the advantages of blocking the sensory nerves that react to TSLP is that it is a more focused approach than stopping the reaction of large numbers of immune cells.
“These itch-sensitive neurons are a small population,” says Bautista. “If we could just block the two percent of neurons that respond to TSLP, we could have a really selective drug that treats chronic itch, but keeps all of the important functions of skin—normal pain function, normal temperature and tactile sensations—and the many parts of the immune system intact.”