Decreased production of semaphorin 3A in the lesional skin of atopic dermatitis

Conflicts of interest: none declared. Sir, We report a potential contribution of semaphorin 3A (Sema3A) to the modulation of epidermal innervation in atopic dermatitis (AD). Cutaneous nerve fibres are present at higher densities in the epidermis of patients with AD. The increase of nerve fibres is partly responsible for the intense itch sensations in atopic skin.1, 2 It is now generally accepted that keratinocyte‐derived nerve growth factor (NGF) is one of the mediators determining skin innervation density in AD.2 Interestingly, Sema3A, which is a diffusible molecule important in repulsive axon guidance during neural development, can inhibit NGF‐induced sprouting of sensory afferents in adult mammalian spinal cord.3, 4 Therefore, Sema3A may be involved in the modulation of epidermal innervation during AD development. However, the relationship between Sema3A and the pathology of AD is currently unclear. Three‐millimetre punch biopsies from normal abdominal skin of nine healthy male volunteers (age range 20–42 years, mean 30·9) and lesional abdominal skin of 11 male patients (age range 20–44 years, mean 31·3) with clinical appearances of chronic AD were used in this study. The mean ± SD visual analogue scale score was 88·6 ± 12·1% in the patients with AD.