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Cutaneous sensitivity modulation by Aquaphilus dolomiae extract‐G3 on in vitro models of neuro‐inflammation
Author(s) -
Lestienne F.,
Viodé C.,
Ceruti I.,
Carrere S.,
BessouTouya S.,
Duplan H.,
CastexRizzi N.
Publication year - 2020
Publication title -
journal of the european academy of dermatology and venereology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.655
H-Index - 107
eISSN - 1468-3083
pISSN - 0926-9959
DOI - 10.1111/jdv.16641
Subject(s) - histamine , inflammation , medicine , in vitro , neurogenic inflammation , human skin , epidermis (zoology) , atopic dermatitis , immunology , in vivo , pharmacology , substance p , chemistry , biology , receptor , biochemistry , neuropeptide , anatomy , microbiology and biotechnology , genetics
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 vitro models evaluated the effect of the original biological extract of Aquaphilus dolomiae extract‐G3 (ADE‐G3) on cutaneous neurogenic inflammation. Results ADE‐G3 significantly inhibited SP‐stimulated release of IL‐1β and TNF‐α 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 to ex vivo human explants, inhibited IL‐8 and histamine release. Conclusions Topically applied ADE‐G3, once formulated, may improve neuro‐inflammation in patients with inflammatory skin disorders.