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<article article-type="research-article" dtd-version="1.3" 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" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">rsp</journal-id><journal-title-group><journal-title xml:lang="ru">Научно-практическая ревматология</journal-title><trans-title-group xml:lang="en"><trans-title>Rheumatology Science and Practice</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1995-4484</issn><issn pub-type="epub">1995-4492</issn><publisher><publisher-name>IMA-PRESS, LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14412/1995-4484-2016-199-205</article-id><article-id custom-type="elpub" pub-id-type="custom">rsp-2217</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ПРОГРЕСС В РЕВМАТОЛОГИИ В XXI ВЕКЕ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>PROGRESS IN RHEUMATOLOGY IN THE XXI CENTURY</subject></subj-group></article-categories><title-group><article-title>Концепция «болезни барьерного органа» в патогенезе спондилоартритов</article-title><trans-title-group xml:lang="en"><trans-title>THE CONCEPT OF BARRIER ORGAN DISEASE IN THE PATHOGENESIS OF SPONDYLOARTHRITIS</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Галушко</surname><given-names>Е. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Galushko</surname><given-names>E. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>учебно-методический отдел с центром информационных технологий</p><p>заведующая отделом, докт. мед. наук</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522 </p></bio><email xlink:type="simple">egalushko@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Гордеев</surname><given-names>А. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Gordeev</surname><given-names>A. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>лаборатория микроциркуляции и воспаления</p><p>ведущий научный сотрудник лаборатории, докт. мед. наук</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522 </p></bio><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБНУ Научно- исследовательский институт ревматологии им. В.А. Насоновой, Москва</institution><country>Россия</country></aff><aff xml:lang="en"><institution>V.A. Nasonova Research Institute of Rheumatology, Moscow</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2016</year></pub-date><pub-date pub-type="epub"><day>19</day><month>07</month><year>2016</year></pub-date><volume>54</volume><issue>2</issue><fpage>199</fpage><lpage>205</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Галушко Е.А., Гордеев А.В., 2016</copyright-statement><copyright-year>2016</copyright-year><copyright-holder xml:lang="ru">Галушко Е.А., Гордеев А.В.</copyright-holder><copyright-holder xml:lang="en">Galushko E.A., Gordeev A.V.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://rsp.mediar-press.net/rsp/article/view/2217">https://rsp.mediar-press.net/rsp/article/view/2217</self-uri><abstract><p>В настоящее время созданы предпосылки для изменения научного взгляда на этиологию и патогенез спондилоартритов (СпА). Важная роль отводится нарушению функционирования и целостности так называемых барьерных органов, выстраивающих защиту человека между его внутренней и внешней средой. Современные данные о клеточно-молекулярных механизмах патогенеза СпА позволяют ревматологам выдвинуть гипотезу о концепции «болезни барьерного органа» как доклинической стадии развития заболеваний, входящих в группу СпА. Существуют основания предполагать, что в этом процессе задействованы индивидуальные генетические и иммунные факторы, приводящие к повреждению поверхностного эпителия слизистых оболочек и эпидермиса, который служит первым защитным барьером врожденного иммунитета и находится в контакте с чрезвычайно большим количеством микроорганизмов (микробиомом) и с патоген-ассоциированными молекулярными структурами. Микробиом может оказывать влияние на доклиническую фазу болезни несколькими способами, в том числе путем изменений состава микрофлоры (дисбиоз), а также действуя в качестве мишеней иммунологической дисрегуляции. </p></abstract><trans-abstract xml:lang="en"><p>There have been now prerequisites for changing the scientific view of the etiology and pathogenesis of spondyloarthritis (SpA). An important role is assigned to the dysfunction and disintegration of the so-called barrier organs that make protection of man between his internal milieu and the environment. An update on cellular and molecular mechanisms in the pathogenesis of SpA permits rheumatologists to offer a hypothesis of the concept of barrier organ disease as a preclinical stage of the diseases included in the SpA group. There is reason to think that this process involves individual genetic and immune factors leading to damage of the superficial epithelium of the mucosal membranes and epidermis that serves as the first protective barrier for innate immunity and is in contact with huge numbers of microorganisms (a microbiome) and with the pathogen-associated molecular patterns. The microbiome may affect the preclinical phase of the disease in several ways, including those to change the composition of the microflora (dysbiosis) and to act as targets for immunological dysregulation. </p></trans-abstract><kwd-group xml:lang="ru"><kwd>спондилоартриты</kwd><kwd>анкилозирующий спондилит</kwd><kwd>микробиом</kwd><kwd>псориаз</kwd><kwd>воспалительные заболевания кишечника</kwd></kwd-group><kwd-group xml:lang="en"><kwd>spondyloarthritis</kwd><kwd>ankylosing spondylitis</kwd><kwd>microbiome</kwd><kwd>psoriasis</kwd><kwd>inflammatory bowel diseases</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Насонов ЕЛ, Александрова ЕН, Новиков АА. Аутоиммунные ревматические заболевания: итоги и перспективы научных исследований. Научно-практическая ревматология. 2015;53(3):230-7. [Nasonov EL, Aleksandrova EN, Novikov AA. 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