Itch-associated neurons in the skin are activated by a commonly expressed protein called periostin. North Carolina State University researchers found that if they blocked periostin receptors on these neurons, it reduced the itching response in mouse models of eczema and atopic dermatitis. The research was published in the journal Cell Reports.
People suffering from eczema face the problem of constant itching that causes all sorts of issues from trouble sleeping to skin infections. If the researchers could turn their findings into a treatment that works on humans, it could change the lives of people living with this condition substantially.
Eczema outbreaks can be triggered by several factors, such as reactions to certain foods, irritants, and allergies. The itching sensation is typically accompanied by redness and dryness as well. All the symptoms are driven by the itch-associated neurons in the skin, which take their cues from clusters of sensory cells based at the root of the spinal nerves called dorsal root ganglia (DRG).
Lead author of the study, Santosh Mishra, who is an assistant professor of neuroscience at NC State, said:
We have found that periostin, a protein that is produced abundantly in the skin as part of an allergic response, can interact directly with sensory neurons in the skin, effectively turning on the itch response. Additionally, we identified the neuronal receptor that is the initial connection between periostin and itch response.
Periostin and its receptor connect the skin directly to the central nervous system. We have identified the first junction in the itch pathway associated with eczema. If we can break that connection, we can relieve the itch.
The team examined the pathway through experiments on mice. They chemically induced the animals to have eczema and then exposed them to common allergens such as dust mites. As the itch response rose, so did the levels of periostin.
There’s another protein – a receptor protein called αvβ3 – that connects periostin with the skin’s sensory neurons, thus driving the exasperated itch response. The team found a way to switch off the receptor and consequently break this chain of command. When they did, it “significantly” reduced the severity of the itching.
