Cutaneous sensitivity modulation by Aquaphilus dolomiae extract-G3 on in vitro models of neuro-inflammation.
Journal
Journal of the European Academy of Dermatology and Venereology : JEADV
ISSN: 1468-3083
Titre abrégé: J Eur Acad Dermatol Venereol
Pays: England
ID NLM: 9216037
Informations de publication
Date de publication:
Aug 2020
Aug 2020
Historique:
received:
13
02
2020
revised:
07
05
2020
accepted:
11
05
2020
entrez:
2
9
2020
pubmed:
2
9
2020
medline:
30
4
2021
Statut:
ppublish
Résumé
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). In vitro models evaluated the effect of the original biological extract of Aquaphilus dolomiae extract-G3 (ADE-G3) on cutaneous neurogenic inflammation. 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. Topically applied ADE-G3, once formulated, may improve neuro-inflammation in patients with inflammatory skin disorders.
Sections du résumé
BACKGROUND
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
OBJECTIVE
In vitro models evaluated the effect of the original biological extract of Aquaphilus dolomiae extract-G3 (ADE-G3) on cutaneous neurogenic inflammation.
RESULTS
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
CONCLUSIONS
Topically applied ADE-G3, once formulated, may improve neuro-inflammation in patients with inflammatory skin disorders.
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
43-48Informations de copyright
© 2020 European Academy of Dermatology and Venereology.
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