The groundbreaking research conducted at North Carolina State University has unveiled the pivotal role of a specific peptide in the onset of atopic dermatitis, commonly known as eczema. This discovery holds immense potential in revolutionizing the treatment landscape for this condition, offering more precise and potent therapeutic interventions.
Atopic dermatitis (AD) manifests as itchy, irritated, and thickened skin at affected sites. A particular peptide, the brain natriuretic peptide (BNP), is elevated in individuals suffering from AD. According to Santosh Mishra, an associate professor of molecular biomedical sciences at NC State and the study’s corresponding author, BNP is produced in sensory neurons—cells responsible for transmitting sensations to the brain through the spinal cord. Previous studies have established BNP’s role in conveying the itch sensation from the skin to the brain. This research aimed to explore BNP’s involvement in activating AD.
The team made a striking observation through a meticulously designed chemically induced mouse model of AD. Mice that lacked BNP did not exhibit the typical signs of AD, such as thickened or irritated skin, and their itching was significantly reduced compared to the control group with BNP. This rigorous approach to the study instils confidence in the validity of our findings.
“Our findings suggest that BNP likely plays a key role in the activation of itch,” Mishra noted. The study then explored the connection between BNP and periostin, aiming to understand the mechanism behind this activation process.
Periostin, a protein that interacts with sensory neurons in the skin to trigger the itch response, is produced in skin cells known as keratinocytes and fibroblasts. Keratinocytes possess receptors for BNP, known as NPR1 receptors. Activation of these receptors by BNP leads to the production of periostin, which activates the itch sensation.
“The intriguing aspect of our findings is that sensory neurons initiate the activation process,” explained Mishra. The neuron releases BNP, which then activates keratinocytes with NPR1 receptors, releasing periostin.
This research not only sheds light on the role of peripheral neurons, but also initiates a cascade of responses in the development of AD. It all starts in the sensory neurons, triggering a series of events. This significant finding not only deepens our understanding of AD, but also opens up a new realm of therapeutic possibilities. For instance, the potential to inhibit BNP’s interaction with NPR1 receptors in the skin could herald a new era in the treatment of AD, instilling hope in the scientific community.
More information: Joshua J. Wheeler et al, Brain Natriuretic Peptide Exerts Inflammation and Peripheral Itch in a Mouse Model of Atopic Dermatitis, Journal of Investigative Dermatology. DOI: 10.1016/j.jid.2023.09.273
Journal information: Journal of Investigative Dermatology Provided by North Carolina State University
