Abstract

The progressively increased incidence of atopic dermatitis among children and increased persistence in adulthood, combined with an inevitably decreased quality of life of patients, determine the relevance of studying the development mechanisms of this disease not only for dermatology but also for the entire health care system. Thus, the prerequisites for the emergence of new pathogenetic concepts and the search for the most effective therapeutic modalities arise. Currently, atopic dermatitis is considered as the interaction of endogenous (impaired immune response and insufficient epidermal barrier function) and exogenous (exposure to allergens, chemical or physical irritants, and microorganisms) factors.
 Environmental factors, such as temperature and humidity, genetic makeup, antibiotic use, and good hygiene, play a critical role in skin microbiome maintenance and stability. Normally, the skin microbiota is mainly formed by bacteria of the genus Staphylococcus, Propionibacterium, Corynebacterium, and Streptococcus. In 70% of patients with atopic dermatitis, colonization of Staphylococcus aureus is observed on the affected skin, whereas on the unaffected skin in 39%, which secondarily contributes to the development of immune imbalance and increased skin xerosis. This fact determines the importance of basic therapy, which, on one hand, helps to strengthen the epidermal barrier, and on the other, normalizes the microbiome of the skin, thereby reducing the colonization of Staphylococcus aureus.
 The normal skin microbiome suppresses the activity of immune-inflammatory responses and regulates pH, lipid synthesis, and transepidermal water loss. Thus, skin microbiome normalization is the key to successful therapy and long-term remission of atopic dermatitis.

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