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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">kurskvest</journal-id><journal-title-group><journal-title xml:lang="ru">Человек и его здоровье</journal-title><trans-title-group xml:lang="en"><trans-title>Humans and their health</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1998-5746</issn><issn pub-type="epub">1998-5754</issn><publisher><publisher-name>Kursk State Medical University</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.21626/vestnik/2022-2/05</article-id><article-id custom-type="elpub" pub-id-type="custom">kurskvest-1027</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>МЕДИКО-БИОЛОГИЧЕСКИЕ НАУКИ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>MEDICOBIOLOGICAL SCIENCES</subject></subj-group></article-categories><title-group><article-title>К вопросу о механизмах повышения проницаемости стенки кишечника при стрессе</article-title><trans-title-group xml:lang="en"><trans-title>On mechanisms of increased intestinal wall permeability under stress</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-1529-6014</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Ворвуль</surname><given-names>Антон Олегович</given-names></name><name name-style="western" xml:lang="en"><surname>Vorvul</surname><given-names>Anton O.</given-names></name></name-alternatives><bio xml:lang="ru"><p>очный аспирант, ассистент кафедры патофизиологии, мл. науч. сотрудник НИИ общей патологии, КГМУ, г. Курск</p></bio><bio xml:lang="en"><p>Full-Time Postgraduate Student, Assistant lecturer at the Department of Pathophysiology, Junior Researcher at the Research Institute of General Pathology, KSMU, Kursk, Russian Federation</p></bio><email xlink:type="simple">vorvul1996@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-7745-2599</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Бобынцев</surname><given-names>Игорь Иванович</given-names></name><name name-style="western" xml:lang="en"><surname>Bobyntsev</surname><given-names>Igor I.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д-р мед. наук, профессор, заведеющий кафедрой патофизиологии, директор НИИ общей патологии, КГМУ, г. Курск</p></bio><bio xml:lang="en"><p>Dr. Sci. (Med.), Professor, Head of the Department of Pathophysiology, Head of the Research Institute of General Pathology, KSMU, Kursk, Russian Federation</p></bio><email xlink:type="simple">bobig@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-2889-155X</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Медведева</surname><given-names>Ольга Анатольевна</given-names></name><name name-style="western" xml:lang="en"><surname>Medvedeva</surname><given-names>Olga A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д-р биол. наук, профессор, заведующий кафедрой микробиологии, вирусологии, иммунологии, КГМУ, г. Курск</p></bio><bio xml:lang="en"><p>Dr. Sci. (Med.), Professor, Head of the Department of Pathophysiology, Head of the Research Institute of General Pathology, KSMU, Kursk, Russian Federation</p></bio><email xlink:type="simple">olgafrida@rambler.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Курский государственный медицинский университет (КГМУ)</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Kursk State Medical University (KSMU)</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2022</year></pub-date><pub-date pub-type="epub"><day>29</day><month>06</month><year>2022</year></pub-date><volume>25</volume><issue>2</issue><fpage>43</fpage><lpage>63</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Ворвуль А.О., Бобынцев И.И., Медведева О.А., 2022</copyright-statement><copyright-year>2022</copyright-year><copyright-holder xml:lang="ru">Ворвуль А.О., Бобынцев И.И., Медведева О.А.</copyright-holder><copyright-holder xml:lang="en">Vorvul A.O., Bobyntsev I.I., Medvedeva O.A.</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://www.kursk-vestnik.ru/jour/article/view/1027">https://www.kursk-vestnik.ru/jour/article/view/1027</self-uri><abstract><p>Одним из проявлений стрессорной реакции в толстой кишке является повышение проницаемости ее стенки вследствие развития воспалительной реакции на фоне изменения нейроэндокринной регуляции и состояния микробиоты. Данные процессы сопровождаются существенными изменениями гуморального гомеостаза и активности клеток, участвующих в развитии воспалительной реакции в стенке толстой кишки. Нами был выполнен обзор литературы, целью которого были анализ и обобщение имеющихся данных исследований о механизмах реализации стресс-индуцированных изменений в кишечнике на молекулярном, клеточном и тканевом уровнях с участием регуляторных систем организма. Поиск научной информации проводили в базах данных Web Of Science, Scopus, ScienceDirect, Medline, Российском индексе научного цитирования (РИНЦ), а также в поисковых системах Google Scholar, PubMed, Semantic Scholar, Taylor &amp; Francis, Wiley Online Library и Bielefeld Academic Search Engine (BASE). Показано, что проницаемость стенки имеет достаточно сложную регуляцию с участием кортикотропин-рилизинг фактора, тучных и дендритных клеток, эозинофилов, макрофагов, субстанции Р, фактора роста нервов, нейротензина, метаболических факторов микробиоты (серотонина, короткоцепочечных жирных кислот, производных индола и конъюгированных жирных кислот), эпигенетических механизмов, оси HES1 (Hairy/Enhancer of Split-1) - GR (глюкокортикоидный рецептор), а также стресс-ассоциированного сигнального пути полярности. При стрессе происходит изменение функционирования данных механизмов, приводящее к повышению проницаемости кишечной стенки. При этом происходит транслокация бактерий из просвета в нижележащие слои, что обусловливает активацию иммунного ответа с последующим развитием воспалительной реакции. Представленные данные свидетельствуют о перспективности и обоснованности разработки методов коррекции стресс-индуцированных сдвигов в толстой кишке путем воздействия на центральные и местные механизмы реализации стрессорной реакции и состояние микробиоты.</p></abstract><trans-abstract xml:lang="en"><p>One of the manifestations of the stress reaction in the colon is an increase in the permeability of its wall due to the development of an inflammatory reaction against the background of changes in neuroendocrine regulation and microbiota state. These processes are accompanied by significant changes in humoral homeostasis and cell activity involved in the development of an inflammatory response in the colon wall. We performed a literature review to analyze and summarize the available research data on the mechanisms of stress-induced changes in the intestine at the molecular, cellular and tissue levels involving the regulatory systems of the body. Scientific information was searched in Web Of Science, Scopus, ScienceDirect, Medline, Russian Science Citation Index (RSCI), as well as in the search engines Google Scholar, PubMed, Semantic Scholar, Taylor &amp; Francis, Wiley Online Library and Bielefeld Academic Search Engine (BASE). Wall permeability has been shown to have a rather complex regulation involving corticotropin-releasing factor, mast cells, dendritic cells, eosinophils, macrophages, Substance P, nerve growth factor, neurotensin, microbiota metabolic factors (serotonin, short-chain fatty acids, indole derivatives and conjugated fatty acids), epigenetic mechanisms, the HES1 (Hairy/Enhancer of Split-1) - GR (glucocorticoid receptor), and the stress-associated polarity signaling pathway. Under stress, there is a change in the functioning of these mechanisms, leading to an increase in the permeability of the intestinal wall. It results in translocation of bacteria from the lumen into the underlying layers which causes activation of the immune response with subsequent development of an inflammatory reaction. The presented data testify to the prospects and validity of the development of methods of correction of stress-induced shifts in the colon by influencing the central and local mechanisms of realization of the stress response and the state of the microbiota.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>стресс</kwd><kwd>проницаемость кишечника</kwd><kwd>иммунные клетки</kwd><kwd>нейропептиды</kwd><kwd>микробиота</kwd><kwd>эпигенетика</kwd><kwd>сигнальные пути</kwd></kwd-group><kwd-group xml:lang="en"><kwd>stress</kwd><kwd>intestinal permeability</kwd><kwd>immune cells</kwd><kwd>neuropeptides</kwd><kwd>microbiota</kwd><kwd>epigenetics</kwd><kwd>signalling pathways</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">Bailey M.T., Dowd S.E., Galley J.D., Hufnagle A.R., Allen R.G., Lyte M. 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