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Atopic dermatitis (AD) is one of the most common itch-inducing allergic skin diseases in humans and animals (1, 2). Interleukin (IL)-31, a cytokine involved in immune response in inflammatory diseases such as AD, has been demonstrated to cause itch by acting on receptors in a subset of transient receptor potential vanilloid (TRPV1) neurons (3-5). We recently identified a small subset of neurons that function as the primary detectors of chemical pruritic stimuli. We showed that the neuropeptide natriuretic polypeptide b (NPPB) is required for the transmission of itch signals and marks the full complement of itch responsive neurons at the periphery (6). However, it remains unknown how itch signals in AD are transmitted by the primary afferents of the sensory neurons in the dorsal root ganglia (DRG) to the spinal cord. This study is aimed to determine if NPPB is involved as a neuropeptide in IL-31-mediated itch in AD via natriuretic polypeptide receptor A (NPRA) in the spinal cord.

Atopic Dermatitis Linked Cytokine Interleukin-31 Induced Itch Mediated via a Neuropeptide Natriuretic Polypeptide B