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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">mimmun</journal-id><journal-title-group><journal-title xml:lang="ru">Медицинская иммунология</journal-title><trans-title-group xml:lang="en"><trans-title>Medical Immunology (Russia)</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1563-0625</issn><issn pub-type="epub">2313-741X</issn><publisher><publisher-name>SPb RAACI</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.15789/1563-0625-FOT-2714</article-id><article-id custom-type="elpub" pub-id-type="custom">mimmun-2714</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>КРАТКИЕ СООБЩЕНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>SHORT COMMUNICATIONS</subject></subj-group></article-categories><title-group><article-title>Особенности цитокинового профиля крови при гастроэзофагеальной рефлюксной болезни у школьников с гастритом и семейным отягощением по язвенной болезни</article-title><trans-title-group xml:lang="en"><trans-title>Features of the blood cytokine profile in gastroesophageal reflux disease in schoolchildren with gastritis and family history of peptic ulcer</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>Поливанова</surname><given-names>Т. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Polivanova</surname><given-names>T. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Поливанова Т.В. – д.м.н., главный научный сотрудник клинического отделения патологии пищеварительной системы у взрослых и детей; доцент кафедры патологической физиологии </p><p>г. Красноярск</p></bio><bio xml:lang="en"><p>Polivanova T.V., PhD, MD (Medicine), Chief Research Associate, Clinical Department of Pathology of the Digestive System in Adults and Children; Associate Professor, Department of Pathological Physiology </p><p>Krasnoyarsk</p></bio><email xlink:type="simple">tamara-polivanova@yandex.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/0000-0002-1410-8747</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Вшивков</surname><given-names>В. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Vshivkov</surname><given-names>V. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Вшивков В.А. – к.м.н., старший научный сотрудник клинического отделения патологии пищеварительной системы у взрослых и детей </p><p>г. Красноярск </p></bio><bio xml:lang="en"><p>Vshivkov V.A., PhD (Medicine), Senior Research Associate, Clinical Department of Pathology of the Digestive System in Adults and Children </p><p>Krasnoyarsk</p></bio><email xlink:type="simple">vitali1983@mail.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Ахметшин</surname><given-names>Т. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Akhmetshin</surname><given-names>T. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Ахметшин Т.Н. – аспирант </p><p>г. Красноярск</p></bio><bio xml:lang="en"><p>Akhmetshin T.N., Postgraduate Student </p><p>Krasnoyarsk</p></bio><email xlink:type="simple">a-thim@mail.ru</email><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Научно-исследовательский институт медицинских проблем Севера – обособленное подразделение ФГБНУ «Федеральный исследовательский центр “Красноярский научный центр Сибирского отделения Российской академии наук”»;&#13;
ФГБОУ ВО «Красноярский государственный медицинский университет имени профессора В.Ф. Войно-Ясенецкого» Министерства здравоохранения РФ</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Research Institute of Medical Problems of the North, Krasnoyarsk Science Center, Siberian Branch, Russian Academy of Sciences;&#13;
Krasnoyarsk State V. Voino-Yasenetsky Medical University</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>Научно-исследовательский институт медицинских проблем Севера – обособленное подразделение ФГБНУ «Федеральный исследовательский центр “Красноярский научный центр Сибирского отделения Российской академии наук”»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Research Institute of Medical Problems of the North, Krasnoyarsk Science Center, Siberian Branch, Russian Academy of Sciences</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2023</year></pub-date><pub-date pub-type="epub"><day>01</day><month>06</month><year>2023</year></pub-date><volume>25</volume><issue>4</issue><fpage>913</fpage><lpage>918</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Поливанова Т.В., Вшивков В.А., Ахметшин Т.Н., 2023</copyright-statement><copyright-year>2023</copyright-year><copyright-holder xml:lang="ru">Поливанова Т.В., Вшивков В.А., Ахметшин Т.Н.</copyright-holder><copyright-holder xml:lang="en">Polivanova T.V., Vshivkov V.A., Akhmetshin T.N.</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.mimmun.ru/mimmun/article/view/2714">https://www.mimmun.ru/mimmun/article/view/2714</self-uri><abstract><p>Гастроэзофагеальная рефлюксная болезнь (ГЭРБ) представляет собой распространенное кислотозависимое заболевание среди населения, в том числе детского с мультифакториальным генезом. Она, как и многие другие кислотозависимые заболевания (язвенная болезнь и др.), ассоциирована с семейной предрасположенностью к заболеванию. Интерес представляет изучение роли цитокинов в регуляции патологии в детском возрасте в зависимости от отягощенности семейного анамнеза по язвенной болезни. Цель – оценить показатели цитокинов в сыворотке крови при семейном отягощении по язвенной болезни у школьников с гастритом, ассоциированным с ГЭРБ. В ходе научного исследования обследовано 142 ребенка с гастроэнтерологическими жалобами в возрасте 7-17 лет. Диагноз «ГЭРБ» выставлялся при наличии еженедельной изжоги в соответствии с глобальным консенсусом по патологии у детей. Всем обследуемым была проведена гастроскопия с взятием биопсийного материала из слизистой желудка и морфологическим подтверждением у них диагноза гастрит в соответствии с Сиднейской классификацией. Методом иммуноферментного анализа получена концентрация цитокинов в сыворотке крови (IL-2, IL-4, IL-6, IL-8, IL-10, IL-18, IL-1β, IFNα, TNFα). При статистической обработке использовались критерии χ2  и Манна–Уитни. Исследования одобрены этическим комитетом и до начала исследования получены информированные согласия пациентов и их родителей. Результаты исследования не показали значимых различий концентрации цитокинов у школьников в зависимости от наличия ГЭРБ. У детей с семейным отягощением по язвенной болезни ГЭРБ определялась чаще (р = 0,054), что, вероятно, является следствием наличия у них повышенного кислотообразования. Отмечены изменения в цитокиновом профиле крови. В течение ГЭРБ при отягощении по язвенной болезни было усиление репликации IL-4 (р = 0,027) и IFNα (р = 0,001). Увеличение IFNα в крови у детей с ГЭРБ при семейном отягощении очевидно направлено на усиление иммунных реакций с участием всего организма на повреждение. Это обусловлено его функциональной ролью – участие в иммунном ответе. Усиление репликации IL-4, очевидно, обеспечивает усиление метаболических, иммунных процессов в организме, направленных на обеспечение оптимизации течения пролиферативных процессов в слизистой пищевода в условиях повышенной секреции соляной кислоты в желудке. Таким образом, при отягощении семейного анамнеза по язвенной болезни у школьников с гастритом, ассоциированным с ГЭРБ наблюдается переход ряда звеньев цитокиновой сети (IL-4, IFNα) на системный уровень регуляции.</p></abstract><trans-abstract xml:lang="en"><p>Gastroesophageal reflux disease (GERD) is a common acid-dependent disease among the population, including children, with multifactorial genesis. It, like many other acid-dependent diseases (peptic ulcer, etc.) is associated with a family predisposition to the disease. Of interest is the study of the role of cytokines in the regulation of pathology in childhood, depending on the severity of a family history of peptic ulcer disease. Aim: to evaluate the levels of cytokines in the blood serum in case of family history of ulcerative diseases in schoolchildren with gastritis associated with GERD. In the course of a scientific study, 142 children with gastroenterological complaints aged 7-17 years were examined. The diagnosis of GERD was made in the presence of weekly heartburn in accordance with the global consensus on pathology in children. All subjects underwent gastroscopy with taking biopsy material from the gastric mucosa and morphological confirmation of their diagnosis of gastritis in accordance with the Sydney classification. The concentration of cytokines in blood serum (IL-2, IL-4, IL-6, IL-8, IL-10, IL-18, IL-1β, IFNα, TNFα) was obtained by enzyme immunoassay. During statistical processing, the χ2  and Mann–Whitney tests were used. The studies were approved by the ethics committee and informed consents of patients and their parents were obtained prior to the start of the study. The results of the study did not show significant differences in the concentration of cytokines in schoolchildren depending on the presence of GERD. In children with a family burden of peptic ulcer, GERD was detected more often (p = 0.054), which is probably a consequence of their increased acid formation. Changes in the cytokine profile of the blood were noted. During GERD, with aggravation of peptic ulcer, there was an increase in the replication of IL-4 (p = 0.027) and IFNα (p = 0.001). The increase in blood IFNα in children with GERD with family burden is obviously aimed at enhancing immune responses involving the whole body to damage. This is due to its functional role – participation in the immune response. Increased replication of IL-4, obviously, provides an increase in metabolic, immune processes in the body aimed at optimizing the course of proliferative processes in the esophageal mucosa under conditions of increased secretion of hydrochloric acid in the stomach. Thus, when a family history of peptic ulcer is aggravated in schoolchildren with gastritis associated with GERD, a number of links in the cytokine network (IL-4, IFNα) move to the systemic level of regulation.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>цитокины</kwd><kwd>дети</kwd><kwd>гастроэзофагеальная рефлюксная болезнь</kwd><kwd>гастрит</kwd><kwd>язвенная болезнь</kwd><kwd>семейная предрасположенность</kwd></kwd-group><kwd-group xml:lang="en"><kwd>cytokines</kwd><kwd>children</kwd><kwd>gastroesophageal reflux disease</kwd><kwd>gastritis</kwd><kwd>peptic ulcer</kwd><kwd>family predisposition</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">Dixon M.F., Genta R.M., Yardley J.H., Correa P. Histological classification of gastritis and Helicobacter pylori infection: an agreement at last? The International Workshop on the Histopathology of Gastritis. 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