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Nerve density in the epidermis is partly involved in itch sensitization in pruritic skin diseases, such as atopic dermatitis (AD). Epidermal innervation is thought to be regulated by the balance between nerve elongation factors (e.g. nerve growth factor) and nerve repulsion factors (e.g. semaphorin 3A). Semaphorin 3A (Sema3A) has been shown to inhibit nerve growth factor (NGF)-induced sprouting of sensory nerves, and epidermal Sema3A levels are lower in AD patients, concomitant with an increase in epidermal nerve density. In addition, treatment with anti-NGF, Sema3A replacement, and several existing treatments, such as ultraviolet-based therapies, normalized the hyperinnervation in AD, resulting in suppression of itching. This review expands knowledge regarding potential therapeutic strategies for ameliorating intractable pruritus in AD.
Tominaga et al. (Sat,) studied this question.