A commonly expressed protein called periostin can directly activate itch-associated neurons in the skin, according to new research.
The researchers found that blocking periostin receptors on these neurons reduced the itch response in a mouse model of atopic dermatitis, or eczema. The findings could have implications for treatment of this condition.
Itch sensations are transmitted from neuronal projections in the skin through the dorsal root ganglia (DRG)—clusters of sensory cells located at the root of the spinal nerves—then to the spinal cord.
“We have found that periostin, a protein that is produced abundantly in skin as part of an allergic response, can interact directly with sensory neurons in the skin, effectively turning on the itch response,” says lead author Santosh Mishra, assistant professor of neuroscience at North Carolina State University. “Additionally, we identified the neuronal receptor that is the initial connection between periostin and itch response.”
The researchers identified a receptor protein called αvβ3, expressed on sensory neurons in skin, as the periostin receptor.
In a chemically-induced mouse model of atopic dermatitis, the team found that exposure to common allergens such as dust mites increased periostin production in skin, exacerbating the itch response. However, when the researchers “turned off” the receptor protein, itch reduced significantly.
“Periostin and its receptor connect the skin directly to the central nervous system,” Mishra says. “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 research appears in Cell Reports.
Funding for the work came from NC State’s startup fund. Additional researchers from NC State, Wake Forest University, and Duke University contributed to the work.
Source: NC State
