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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="en"><front><journal-meta><journal-id journal-id-type="publisher-id">nnp</journal-id><journal-title-group><journal-title xml:lang="en">Neurology, Neuropsychiatry, Psychosomatics</journal-title><trans-title-group xml:lang="ru"><trans-title>Неврология, нейропсихиатрия, психосоматика</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2074-2711</issn><issn pub-type="epub">2310-1342</issn><publisher><publisher-name>"IMA-Press", LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14412/2074-2711-2018-1S-38-45</article-id><article-id custom-type="elpub" pub-id-type="custom">nnp-907</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="en"><subject>ORIGINAL INVESTIGATIONS</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ОРИГИНАЛЬНЫЕ ИССЛЕДОВАНИЯ И МЕТОДИКИ</subject></subj-group></article-categories><title-group><article-title>The role of neuroinflammation in the pathogenesis of epilepsy</article-title><trans-title-group xml:lang="ru"><trans-title>Роль нейровоспаления в патогенезе эпилепсии</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>Липатова</surname><given-names>Л. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Lipatova</surname><given-names>L. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>192019, Санкт-Петербург, ул. Бехтерева, 3</p></bio><bio xml:lang="en"><p>3, Bekhterev St., Saint Petersburg 192019</p></bio><email xlink:type="simple">epilepsy-net@ya.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>Серебряная</surname><given-names>Н. Б.</given-names></name><name name-style="western" xml:lang="en"><surname>Serebryanaya</surname><given-names>N. B.</given-names></name></name-alternatives><bio xml:lang="ru"><p>191015, Санкт-Петербург, ул. Кирочная, 41</p></bio><bio xml:lang="en"><p>41, Kirochnaya St., Saint Petersburg 191015</p></bio><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Сивакова</surname><given-names>Н. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Sivakova</surname><given-names>N. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>192019, Санкт-Петербург, ул. Бехтерева, 3</p></bio><bio xml:lang="en"><p>3, Bekhterev St., Saint Petersburg 192019</p></bio><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБУ «Национальный медицинский исследовательский центр психиатрии и неврологии им. В.М. Бехтерева» Минздрава России</institution><country>Россия</country></aff><aff xml:lang="en"><institution>V.M. Bekhterev National Medical Research Center of Psychiatry and Neurology, Ministry of Health of Russia</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>ГБОУ ВПО «Северо-Западный государственный медицинский университет им. И.И. Мечникова» Минздрава России</institution><country>Россия</country></aff><aff xml:lang="en"><institution>I.I. Mechnikov North-Western State Medical University, Ministry of Health of Russia</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2018</year></pub-date><pub-date pub-type="epub"><day>17</day><month>07</month><year>2018</year></pub-date><volume>10</volume><issue>1S</issue><issue-title>СПЕЦВЫПУСК: ЭПИЛЕПСИЯ</issue-title><fpage>38</fpage><lpage>45</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Lipatova L.V., Serebryanaya N.B., Sivakova N.A., 2018</copyright-statement><copyright-year>2018</copyright-year><copyright-holder xml:lang="ru">Липатова Л.В., Серебряная Н.Б., Сивакова Н.А.</copyright-holder><copyright-holder xml:lang="en">Lipatova L.V., Serebryanaya N.B., Sivakova N.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://nnp.ima-press.net/nnp/article/view/907">https://nnp.ima-press.net/nnp/article/view/907</self-uri><abstract><p>Over the past decade, there has been a large amount of evidence indicating neuroendocrine, biochemical, and immune disorders in many acute and chronic central nervous system (CNS) diseases,  including epilepsy, which made the authors consider the  inflammatory theory of epileptogenesis. The chronic inflammatory  process in epilepsy is believed to be facilitated by the activation of  microglia and astrogliosis, which are accompanied by neuronal  damage. The main postulate of this type of investigation is the  assumption that the basis for CNS inflammation is blood-brain barrier (BBB) damage. Cytokines are presumed to play the  greatest role in this process, mainly because they are natural pro-  and anticonvulsants.</p><sec><title>Patients and methods</title><p>Patients and methods. Examinations were made in 160 patients with epilepsy (drug-resistant epilepsy (n = 80) and controlled epilepsy (n = 80)) and 30 apparently healthy donors. The blood and  cerebrospinal fluid (CSF) levels of the cytokines interleukin (IL)-1β,  IL-2, IL-6, IL-8, IL-10, tumor necrosis factor-α (TNF-α), IL-1 receptor  antagonist (IL-1RA), soluble IL-2 receptor (sIL-2R), brain- derived neurotrophic factor (BDNF), S100b protein, С-reactive  protein (CRP), and albumins were analyzed using a solid-phase  enzyme-linked immunoabsorbent assay. Statistical analysis was performed using Student’s t-test and Mann-Whitney U-test.  Differences at p &lt;0.05 were regarded as statistically significant.</p></sec><sec><title>Results and discussion</title><p>Results and discussion. The investigation showed that the patients with epilepsy had a substantially impaired plasma cytokine profile: higher levels of proinflammatory cytokines, such as Il-1β, IL-8, and  TNF, and a lower concentration of IL-1 RA. The elevated CSF levels of the cytokines Il-1β and IL8 in patients with epilepsy suggest that  BBB is impaired and a systemic inflammatory process exists while  the absence of IL-1RA indicates that protective inflammation factors  in blood and CSF are reduced.</p></sec></abstract><trans-abstract xml:lang="ru"><p>За последние десятилетия накоплен большой фактический материал, свидетельствующий о нейроэндокринных, биохимических, иммунных нарушениях при многих острых и  хронических заболеваниях центральной нервной системы (ЦНС), включая эпилепсию, что  способствовало рассмотрению воспалительной теории эпилептогенеза. Считается, что  хронизации воспалительного процесса при эпилепсии способствуют активация микроглии и  астроглиоз, сопровождающиеся повреждением нейронов. Основным постулатом такого рода  работ является положение о том, что в основе воспаления в ЦНС лежит повреждение  гематоэнцефалического барьера (ГЭБ). Предполагается, что в этом процессе наибольшую  роль играют цитокины, главным образом потому, что они являются природными про- и  антиконвульсантами.</p><sec><title>Пациенты и методы</title><p>Пациенты и методы. Обследовано 160 больных эпилепсией (80 – с фармакорезистентной эпилепсией, 80 – с контролируемой эпилепсией) и 30 практически здоровых доноров.  Производилась оценка уровней цитокинов в плазме и цереброспинальной жидкости (ЦСЖ) – интерлейкина 1β (ИЛ1β), ИЛ2, ИЛ6, ИЛ8, ИЛ10, фактора некроза опухоли α (ФНОα),  рецепторного антагониста ИЛ1β (RAIL1), растворимого рецептора ИЛ2 (рИЛ2Р),  нейротрофического фактора мозга (BDNF), белка S-100 (S100b), С-реактивного белка (СРБ), альбуминов методом твердофазного иммуноферментного анализа. Статистический анализ  проводился с помощью t-критерия Стьюдента и U-критерия Манна–Уитни. Различия считались статистически значимыми при р&lt;0,05.</p></sec><sec><title>Результаты и обсуждение</title><p>Результаты и обсуждение. Проведенное исследование показало, что у больных эпилепсией имеется существенное нарушение профиля цитокинов в плазме крови:  повышены уровни провоспалительных цитокинов (ИЛ1β, ИЛ8 и ФНОα) и снижена  концентрация RAIL1. Наличие повышенного уровня цитокинов ИЛ1β и ИЛ8 в ЦСЖ у больных эпилепсией свидетельствует о нарушении ГЭБ и существовании системного воспалительного процесса, а отсутствие RAIL1 – о снижении защитных факторов воспаления в крови и ликворе.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>эпилепсия</kwd><kwd>воспаление</kwd><kwd>нейровоспаление</kwd><kwd>цитокины.</kwd></kwd-group><kwd-group xml:lang="en"><kwd>epilepsy</kwd><kwd>inflammation</kwd><kwd>neuroinflammation</kwd><kwd>cytokines</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">Scheffer IE, French J, Hirsch E, et al. 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