Cutaneous sensitivity modulation byAquaphilus dolomiaeextract-G3 onin vitromodels of neuro-inflammation

Background Inflammatory skin disorders, including atopic dermatitis (AD), associated pruritus and sensitive skin, have a complex multifactorial pathogenesis including neurogenic inflammation involving the release in blood and skin of neurotransmitters such as substance P (SP). Aims and Methods In vitromodels evaluated the effect of the original biological extract ofAquaphilus dolomiaeextract-G3 (ADE-G3) on cutaneous neurogenic inflammation. Results ADE-G3 significantly inhibited SP-stimulated release of IL-1 beta and TNF-alpha from normal human epidermal keratinocytes; significantly and dose-dependently inhibited SP-stimulated activation of human mast cells; significantly inhibited veratridine-stimulated release of SP from human sensory neurons; modulated expression of genes involved in lipid synthesis, innate immunity, corneocyte scaffolding and epidermal differentiation in a histamine-sensitized reconstructed human epidermis model; and, when applied topically toex vivohuman explants, inhibited IL-8 and histamine release. Conclusions Topically applied ADE-G3, once formulated, may improve neuro-inflammation in patients with inflammatory skin disorders.