cientists have finally scratched the surface about why, exactly, poison ivy makes people so itchy.
About 10 million Americans suffer from an allergic reaction to poison ivy every year. It’s a serious threat to firefighters, farmers, and others who work outdoors; poison ivy is to blame for 10 percent of the US Forest Service’s lost-time injuries. Now, researchers looking for clues about how poison ivy causes allergic reactions have stumbled upon a key chemical that offers some answers — and points to a potential treatment.
“It’s the most common cause of environmental contact allergy,” said Sven-Eric Jordt, an inflammation researcher at Duke University and the lead author of the new research, published Monday in the Proceedings of the National Academy of Sciences.
The major allergen found in poison ivy is a chemical called urushiol, which is found in the sap of poison ivy plants and its cousins, poison oak and poison sumac. Between 50 and 75 percent of people are allergic to urushiol.
But it’s been difficult for scientists to study, in part because animal models haven’t been useful. So Jordt and his colleagues developed a new mouse model of poison ivy allergy that focused on immune mediators, which are responsible for detecting when the skin comes into contact with an allergen.
“The immune system has a memory of being in contact with this before and then fiercely defends against it,” he explained. “It produces this very exaggerated response.”
For poison ivy, that means an irritating, persistent itch, rashes, and swelling of the skin. That can cause an uncontrollable urge to scratch, which in turn worsens the rash. A run-in with poison ivy can quickly devolve into a painful, scratchy cycle that can last for weeks and, in some cases, cause skin infections that require antibiotics.
Minuscule proteins are triggering that immune response — and, it turns out, one of them is driving the sensation to itch, too.
“One of these proteins, IL-33, acts on the very fine nerve endings in the skin that make us sense itch,” Jordt explained. When an allergic person comes into contact with urushiol, that protein fires off a signal to the brain in much the same way it would signal temperature or pressure.
IL-33 has previously been investigated for its role in food allergies, anaphylaxis, and other inflammatory responses. Two companies, AnaptysBio and Genentech, are currently conducting clinical trials for IL-33 blockers as potential asthma treatments.
That finding gives Jordt and his colleagues a jumping-off point to investigate potential treatments that clamp down on IL-33’s response in poison ivy allergies.
“We used an antibody that blocks that signaling response,” Jordt said. “And when we interfere with this signal, then the itch is alleviated.”
They also discovered a binding protein that’s present in the nerves that trigger itch. Another antibody that blocked that receptor seemed to shut off the itch response, too.
There’s still much more work to be done — it’s not yet clear whether IL-33 works in the same way in human skin cells that it does in mice. Jordt is currently working with dermatologists to collect skin samples of poison ivy patients to confirm IL-33 is present.
“If we can confirm that, it would be a good sign that these treatments might work,” he said.