Official websites use. Share sensitive information only on official, secure websites. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. Atopic dermatitis AD is a common skin disease characterized by recurrent pruritic inflammatory skin lesions resulting from structural and immune defects of the skin barrier.
The present study evaluated the anti-inflammatory, antipruritic, and immunomodulatory properties of ES0, an original biological extract of A. An ES0 extract containing periplasmic and membrane proteins, peptides, lipopolysaccharides, and exopolysaccharides was obtained from A. The effects of the extract on pruritus and inflammatory mediators and immune mechanisms were evaluated by using various AD cell models and assays.
Lastly, ES0 markedly activated innate immunity through toll-like receptor TLR 2, TLR4, and TLR5 activation in recombinant human embryonic kidney cells and through antimicrobial peptide induction psoriasin, human beta-defensin-2, and cathelicidin , mainly through TLR5 activation in normal human keratinocytes.
Overall, these in vitro results confirm the marked regulatory activity of this A. Keywords: atopic dermatitis, inflammation, anti-inflammation, in vitro and in vivo activities, barrier function, microorganism. Atopic dermatitis AD is a common chronic skin disease characterized by recurrent pruritic inflammatory skin lesions resulting from a compromised skin barrier caused by genetically and environmentally determined structural defects and immune dysregulation.
From various studies, it was found that keratinocytes express toll-like receptors TLRs , which are a family of evolutionary conserved pattern recognition receptors PRRs involved in innate immunity. Based on its distinctive phenotypic and genotypic characteristics, this newly identified strain was assigned to a new genus, as a representative of a novel species called Aquaphilus dolomiae. In the present study, the activity of ES0, an original biological extract of A.
