Scratching beneath the surface for new ways to reduce chronic itching

‘The symptoms of chronic itch can be more bothersome than the underlying disease,’ says one researcher who is working on ways to block the signal

Photograph: Thinkstock

Photograph: Thinkstock

 

Here’s an experiment: see if you can read this article to the end without scratching an itch. It might be a bit of fun here, but for some people a persistent or chronic itch is no laughing matter, and that is why Prof Martin Steinhoff is deciphering the “conversation” in our skin that makes some itches so difficult to scratch.

The type of itch that interests him is not the acute annoyance triggered by, perhaps, an insect landing on your arm. He is focusing on the types of itch that crop up in many skin conditions and beyond, including eczema, psoriasis, kidney and liver conditions, some types of cancer and as a result of ageing.

“As with chronic pain, the symptoms of chronic itch can be very debilitating and can sometimes be even more bothersome than the underlying disease,” says Steinhoff, who is professor of dermatology at University College Dublin.

Part of what makes the itch persist is the communication in the skin between the immune system and the nerves that relay the “itching” message to the brain, he says. “Skin cells and immune cells within the skin can release chemicals called cytokines and chemokines; these can communicate with nerves, and this makes you want to scratch.”

Knowing how these chemical messengers in the skin work together could help uncover new ways to cut the communication, says Steinhoff. “We want to better figure out what specific messengers are being sent by the immune system in patients with different types of itch, and what receptors on the nerves are picking up those messages,” he says.

“If you can identify the pathways that are responsible to mediate chronic itch in subtypes of patients, perhaps renal itch, liver itch, leukaemia itch, skin disease itch, then you can develop first-line therapies in the future to alleviate the itch.”

One of the best known itch- triggering “master signals” is histamine, which gets released by immune cells, but not all itches are blocked by antihistamines, and Steinhoff says this is why we need to look for other pathways to itchiness.

A prime candidate on these pathways is another chemical messenger, interleukin-31. Steinhoff and his colleagues recently described a mechanism by which this protein can broker communication between the immune and nervous systems in the skin.

Steinhoff, who directs the Charles Institute of Dermatology at UCD, was recently awarded funding under a Science Foundation Ireland programme to tease out the immune and sensory cross-talk that drives itch. It’s early-stage research, but he believes it will identify new ways of reducing itchiness.

“There’s huge interest in conditions such as eczema, where you have a big immune component and a big itch component, and we want to find out how these signals are getting perpetuated,” he says. “For this and other conditions where itch is a problem, we want to pinpoint where we can block these pathways and thereby block the itch.”

So . . . did you scratch?

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