Pinpointing BNP’s Role in AD
The results of a new study show that BNP likely plays a role in itch activation.
The brain natriuretic peptide (BNP) may play a role in activating atopic dermatitis, according to new research in mice.
“BNP is expressed in sensory neurons, the neurons responsible for conveying sensation to the brain via the spinal cord,” says Santosh Mishra, associate professor of molecular biomedical sciences at North Carolina State University and corresponding author of the work. “We know from previous work that BNP helps translate the sensation of itch from the skin to the brain. In this work we wanted to see if BNP was involved in activating AD.” BNP is elevated in patients with AD.
In a chemically induced mouse model of AD, the researchers saw that mice without BNP did not exhibit the thickened or irritated skin commonly associated with AD, and their itching was reduced compared with control mice who did have BNP.
“The results show that BNP likely plays a role in itch activation,” Mishra says. “We next looked at BNP’s relationship to periostin, to see if we could determine how that activation takes place.”
Produced in keratinocytes and fibroblasts, periostin can interact with sensory neurons in skin to activate itch response. Keratinocytes, in turn, have receptors for BNP, which are called NPR1 receptors. When the BNP receptors are activated, periostin is produced and itch can be turned on.
“The interesting thing here is that the sensory neurons are the activator,” Mishra says. The neuron releases BNP, which activates keratinocytes with the NPR1 receptor, which then release the periostin.
“This work shows that peripheral neurons, not just central neurons, are playing a role in AD – it begins in the sensory neurons, and cascades from there,” Mishra adds. “It also points to some potential therapeutic strategies, such as blocking BNP’s ability to bind to NPR1 receptors in the skin.”
The research appears as a letter to the editor in the Oct. 11 issue of the Journal of Investigative Dermatology.