Abstract

The skin in patients with atopic dermatitis (AD) is constantly colonized by S. aureus, in part due to a deficit in epidermal antimicrobial peptides. S. aureus can cause secondary infections but is also involved in the occurrence and severity of the inflammatory flares of AD. Thus, the diversity of skin microbiota is abnormal in AD. Dynamic studies of the microbiota showed that the prevalence of staphylococcae sp. is further increased during flares of AD. This dysbiosis leads to an increase in inflammatory reactions in which staphylococcal toxins play an important role. Changes in the gut microbiota also play a role in the early maturation of the immune system and the occurrence of allergic reactions. Attempts in the modulation of skin microbiota have recently been made showing that a cream containing a lysate of a non pathogenic Gram negative bacteria, V. filiformis, is capable of improving the manifestations of AD. These effects may be driven by a regulation of skin innate immunity through Toll like receptors (TLR-2), the secretion of IL-10 and the induction of regulatory T cells.

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