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<article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="review-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Russian Journal of Allergy</journal-id><journal-title-group><journal-title xml:lang="en">Russian Journal of Allergy</journal-title><trans-title-group xml:lang="ru"><trans-title>Российский Аллергологический Журнал</trans-title></trans-title-group></journal-title-group><issn publication-format="print">1810-8830</issn><issn publication-format="electronic">2686-682X</issn><publisher><publisher-name xml:lang="en">Publishing House ABV Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">1496</article-id><article-id pub-id-type="doi">10.36691/RJA1496</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Reviews</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Научные обзоры</subject></subj-group><subj-group subj-group-type="article-type"><subject>Review Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">Altered skin microbiome: The most important symptom of atopic dermatitis</article-title><trans-title-group xml:lang="ru"><trans-title>Изменённый микробиом кожи ― важнейший признак атопического дерматита</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-3261-6718</contrib-id><contrib-id contrib-id-type="spin">5476-8497</contrib-id><name-alternatives><name xml:lang="en"><surname>Tamrazova</surname><given-names>Olga B.</given-names></name><name xml:lang="ru"><surname>Тамразова</surname><given-names>Ольга Борисовна</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>MD, Dr. Sci. (Med), Professor</p></bio><bio xml:lang="ru"><p>д.м.н., профессор</p></bio><email>anait_tamrazova@mail.ru</email><xref ref-type="aff" rid="aff1"/><xref ref-type="aff" rid="aff2"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-3004-6646</contrib-id><name-alternatives><name xml:lang="en"><surname>Glukhova</surname><given-names>Evgeniya A.</given-names></name><name xml:lang="ru"><surname>Глухова</surname><given-names>Евгения Александровна</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>evgeniya.shmeleva1994@yandex.ru</email><xref ref-type="aff" rid="aff1"/><xref ref-type="aff" rid="aff3"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-4672-697X</contrib-id><contrib-id contrib-id-type="spin">1563-1190</contrib-id><name-alternatives><name xml:lang="en"><surname>Tamrazova</surname><given-names>Anait V.</given-names></name><name xml:lang="ru"><surname>Тамразова</surname><given-names>Анаит Вардановна</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="ru"><p> </p>
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</p><p> </p>
</bio><email>anaittamrazova@gmail.com</email><xref ref-type="aff" rid="aff4"/><xref ref-type="aff" rid="aff5"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-3278-4797</contrib-id><contrib-id contrib-id-type="spin">3677-5969</contrib-id><name-alternatives><name xml:lang="en"><surname>Dubovets</surname><given-names>Natalia F.</given-names></name><name xml:lang="ru"><surname>Дубовец</surname><given-names>Наталия Федоровна</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>skorpionka_n@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">Moscow’s Healthcare Department Children Hospital of Z.A. Bashlyaeva</institution></aff><aff><institution xml:lang="ru">Детская городская клиническая больница имени З.А. Башляевой Департамента здравоохранения города Москвы</institution></aff></aff-alternatives><aff-alternatives id="aff2"><aff><institution xml:lang="en">Peoples’ Friendship University of Russia</institution></aff><aff><institution xml:lang="ru">Российский университет дружбы народов</institution></aff></aff-alternatives><aff-alternatives id="aff3"><aff><institution xml:lang="en">Federal Research Center of Nutrition and Biotechnology</institution></aff><aff><institution xml:lang="ru">Федеральный исследовательский центр питания, биотехнологии и безопасности пищи</institution></aff></aff-alternatives><aff-alternatives id="aff4"><aff><institution xml:lang="en">Central State Medical Academy of Department of Presidential Affairs</institution></aff><aff><institution xml:lang="ru">Центральная государственная медицинская академия Управления делами Президента Российской Федерации</institution></aff></aff-alternatives><aff-alternatives id="aff5"><aff><institution xml:lang="en">Krasnogorsk Dermatovenerologic Dispensary</institution></aff><aff><institution xml:lang="ru">Красногорский кожно-венерологический диспансер</institution></aff></aff-alternatives><pub-date date-type="preprint" iso-8601-date="2021-12-22" publication-format="electronic"><day>22</day><month>12</month><year>2021</year></pub-date><pub-date date-type="pub" iso-8601-date="2021-12-14" publication-format="electronic"><day>14</day><month>12</month><year>2021</year></pub-date><volume>18</volume><issue>4</issue><issue-title xml:lang="en"/><issue-title xml:lang="ru"/><fpage>107</fpage><lpage>115</lpage><history><date date-type="received" iso-8601-date="2021-11-09"><day>09</day><month>11</month><year>2021</year></date><date date-type="accepted" iso-8601-date="2021-12-10"><day>10</day><month>12</month><year>2021</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2021, Pharmarus Print Media</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2021, Фармарус Принт Медиа</copyright-statement><copyright-year>2021</copyright-year><copyright-holder xml:lang="en">Pharmarus Print Media</copyright-holder><copyright-holder xml:lang="ru">Фармарус Принт Медиа</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/" start_date="2024-01-14"/></permissions><self-uri xlink:href="https://rusalljournal.ru/raj/article/view/1496">https://rusalljournal.ru/raj/article/view/1496</self-uri><abstract xml:lang="en"><p>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.</p> <p>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 <italic>Staphylococcus</italic>, <italic>Propionibacterium</italic>, <italic>Corynebacterium</italic>, and <italic>Streptococcus</italic>. In 70% of patients with atopic dermatitis, colonization of <italic>Staphylococcus aureus</italic> 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 <italic>Staphylococcus aureus</italic>.</p> <p>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.</p></abstract><trans-abstract xml:lang="ru"><p>Прогрессирующий рост заболеваемости атопическим дерматитом среди детей, нарастание персистенции во взрослом возрасте при неизбежном снижении качества жизни пациентов обусловливают актуальность изучения механизмов развития данного заболевания не только для дерматологии, но и всего здравоохранения в целом. Таким образом, возникают предпосылки к появлению новых концепций патогенеза и поиска наиболее эффективных терапевтических возможностей. На данный момент атопический дерматит рассматривают как взаимодействие эндогенных (нарушенный иммунный ответ, недостаточность функции эпидермального барьера) и экзогенных (воздействие аллергенов, химических или физических раздражителей, микроорганизмы) факторов.</p> <p>Факторы окружающей среды, такие как температура и влажность, генетические особенности организма, использование антибиотиков и соблюдение гигиены, играют решающую роль в поддержании и стабильности микробиома кожи. В норме микробиота кожного покрова образована в основном бактериями рода <italic>Staphylococcus</italic>, <italic>Propionibacterium</italic>, <italic>Corynebacterium</italic> и <italic>Streptococcus</italic>. У пациентов с атопическим дерматитом поражённая кожа колонизирована <italic>Staphylococcus aureus </italic>в 70% случаев, непоражённая кожа ― в 39%, что свидетельствует о вторичных причинах иммунного дисбаланса и усиления ксероза кожи. Данный факт обусловливает важность применения базовой терапии, которая, с одной стороны, способствует укреплению эпидермального барьера, с другой ― нормализует микробиом кожного покрова, снижая колонизацию золотистого стафилококка.</p> <p>Нормальный микробиом кожи подавляет активность иммунных воспалительных реакций, регулирует pH, синтез липидов и транэпидермальную потерю воды. Таким образом, нормализация микробиома кожи является залогом успешной терапии и длительной ремиссии атопического дерматита.</p></trans-abstract><kwd-group xml:lang="en"><kwd>atopic dermatitis</kwd><kwd>skin dysbiosis</kwd><kwd>microbiome</kwd><kwd>Staphylococcus aureus</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>атопический дерматит</kwd><kwd>дисбиоз кожи</kwd><kwd>микробиом</kwd><kwd>золотистый стафилококк</kwd></kwd-group><funding-group><funding-statement xml:lang="en">The work was written with the support of the company "L'Oréal"</funding-statement><funding-statement xml:lang="ru">Поисково-аналитическая работа проведена при поддержке компании L’Oréal</funding-statement></funding-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><citation-alternatives><mixed-citation xml:lang="en">Frazier W, Bhardwaj N. Atopic dermatitis: diagnosis and treatment. 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