<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE article PUBLIC "-//NLM//DTD JATS (Z39.96) Journal Publishing DTD v1.3 20210610//EN" "JATS-journalpublishing1-3.dtd">
<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">10.15789/1563-0625-2016-2-187-192</article-id><article-id custom-type="elpub" pub-id-type="custom">mimmun-1003</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>СУБПОПУЛЯЦИОННЫЙ СОСТАВ ЛИМФОЦИТОВ У МОЛОДЫХ МУЖЧИН С МЕТАБОЛИЧЕСКИМ СИНДРОМОМ</article-title><trans-title-group xml:lang="en"><trans-title>LYMPHOCYTE SUBPOPULATION PROFILE IN YOUNG MEN WITH METABOLIC SYNDROME</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>Сумеркина</surname><given-names>В. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Sumerkina</surname><given-names>V. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.м.н., старший научный сотрудник Центральной научно-исследовательской лаборатории,</p><p>454091, г. Челябинск, ул. 3-го Интернационала, 130, кв. 4</p></bio><bio xml:lang="en"><p>PhD (Medicine), Senior Research Associate, Central Research Laboratory,</p><p>454091, Chelyabinsk, 3rd International str., 130, apt 4</p></bio><email xlink:type="simple">veronika.sumerkina@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>Телешева</surname><given-names>Л. Ф.</given-names></name><name name-style="western" xml:lang="en"><surname>Telesheva</surname><given-names>L. F.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д.м.н., профессор, кафедра микробиологии, вирусологии, иммунологии и клинической лабораторной диагностики,</p><p>г. Челябинск</p></bio><bio xml:lang="en"><p>PhD, MD (Medicine), Professor, Department of Microbiology, Virology, Immunology and Clinical Laboratory Diagnostics,</p><p>Chelyabinsk</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Головнева</surname><given-names>Е. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Golovneva</surname><given-names>E. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д.м.н., профессор, кафедра нормальной физиологии,</p><p>г. Челябинск</p></bio><bio xml:lang="en"><p>PhD, MD (Medicine), Professor, Department of Normal Physiology,</p><p>Chelyabinsk</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Квятковская</surname><given-names>С. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Kvyatkovskaya</surname><given-names>S. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.м.н., научный сотрудник НИИ иммунологии,</p><p>г. Челябинск</p></bio><bio xml:lang="en"><p>PhD (Medicine), Research Associate, Institute of Immunology,</p><p>Chelyabinsk</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Дворчик</surname><given-names>Е. Е.</given-names></name><name name-style="western" xml:lang="en"><surname>Dvorchik</surname><given-names>E. E.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.м.н., научный сотрудник НИИ иммунологии,</p><p>г. Челябинск</p></bio><bio xml:lang="en"><p>PhD (Medicine), Research Associate, Institute of Immunology,</p><p>Chelyabinsk</p></bio><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru">ГБОУ ВПО «Южно-Уральский государственный медицинский университет» Министерства здравоохранения РФ<country>Россия</country></aff><aff xml:lang="en">South Ural State Medical University, Ministry of Healthcare of the Russian Federation<country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2016</year></pub-date><pub-date pub-type="epub"><day>15</day><month>04</month><year>2016</year></pub-date><volume>18</volume><issue>2</issue><fpage>187</fpage><lpage>192</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Сумеркина В.А., Телешева Л.Ф., Головнева Е.С., Квятковская С.В., Дворчик Е.Е., 2016</copyright-statement><copyright-year>2016</copyright-year><copyright-holder xml:lang="ru">Сумеркина В.А., Телешева Л.Ф., Головнева Е.С., Квятковская С.В., Дворчик Е.Е.</copyright-holder><copyright-holder xml:lang="en">Sumerkina V.A., Telesheva L.F., Golovneva E.S., Kvyatkovskaya S.V., Dvorchik E.E.</copyright-holder><license 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/1003">https://www.mimmun.ru/mimmun/article/view/1003</self-uri><abstract><p>Метаболический синдром представляет собой субклинический хронический воспалительный процесс. Литературные данные о состоянии иммунного статуса при метаболическом синдроме неоднозначны. Кроме того, гендерные особенности метаболического синдрома освещены недостаточно.</p><p>Цель исследования – определить особенности субпопуляционного состава лимфоцитов у молодых мужчин с метаболическим синдромом и сочетанием абдоминального ожирения с артериальной гипертензией. В исследование было включено 77 мужчин в возрасте 20-45 лет. Мужчины были распределены на 4 группы, сопоставимые по возрасту: 1 группа – контрольная группа (практически здоровые мужчины); 2 группа – мужчины с изолированным абдоминальным ожирением; 3 группа – мужчины с сочетанием абдоминального ожирения и артериальной гипертензии; 4 группа – мужчины с метаболическим синдромом. Методом проточной цитометрии были выделены и проанализированы субпопуляции лимфоцитов: Т-лимфоциты, Т-хелперы, Т-цитотоксические, TNK-лимфоциты, NK-лимфоциты, В-лимфоциты, лимфоциты с фенотипами CD3+CD25+ и СD3+HLADR+. Наличие изолированного абдоминального ожирения у мужчин сопровождалось повышением относительного содержания Т-лимфоцитов, относительного содержания клеток с фенотипом СD3+CD8+ и СD3+CD25+, а также абсолютного количества В-лимфоцитов. Сочетание абдоминального ожирения с артериальной гипертензией у мужчин характеризовалось снижением соотношения Т-хелперов и Т-цитотоксических лимфоцитов за счет уменьшения относительного содержания CD3+CD4+ и повышения CD3+CD8+ лимфоцитов. Количество Т-хелперов было достоверно ниже, чем в группе контроля и при изолированном абдоминальном ожирении. Количество Т-лимфоцитов с фенотипом CD3+HLA-DR+ более чем в 2 раза превышало аналогичный показатель в группе практически здоровых мужчин.</p></abstract><trans-abstract xml:lang="en"><p>Metabolic syndrome is a chronic subclinical inflammation. Published data on the immune state in metabolic syndrome are inconsistent, and, moreover, the gender features of metabolic syndrome are not described in details. The purpose of the study was to determine subpopulation profile of peripheral lymphocytes in young men with metabolic syndrome, as well as in cases of combined abdominal obesity and hypertension. The study included seventy-seven men aged 20-45 years. The men were divided into four groups matched by age: Group 1 represented healthy controls; group 2 included male patients with isolated abdominal obesity; group 3 consisted of males with a combination of abdominal obesity and hypertension; group 4, males with metabolic syndrome. The major lymphocyte subpopulations were isolated and analyzed by flow cytometry, i.e. T lymphocytes, T helpers, T-cytotoxic cells, TNK-lymphocytes, NK-cells, B-cells, as well as CD3+CD25+ and CD3+HLADR+ lymphocytes. In male patients with isolated abdominal obesity, we revealed increased relative contents of T lymphocytes, and increased proportion of the cells with CD3+CD8+, CD3+CD25+ phenotypes and higher B-cell numbers. A combination of abdominal obesity with hypertension in men was characterized by decreased ratio of T-helper/T-cytotoxic lymphocytes, due to reduced relative contents of CD3+CD4+ cells and increase in CD3+CD8+ lymphocytes. The numbers of T-helper cells in this group were significantly lower than in controls and among patients with isolated abdominal obesity. The number of T-cells with CD3+HLADR+ phenotype proved to be 2-fold higher than in the group of healthy male controls.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>метаболический синдром</kwd><kwd>субпопуляции лимфоцитов</kwd><kwd>абдоминальное ожирение</kwd><kwd>артериальная гипертензия</kwd></kwd-group><kwd-group xml:lang="en"><kwd>lymphocyte subpopulations</kwd><kwd>abdominal obesity</kwd><kwd>hypertension</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">Литвинова Л.С., Кириенкова Е.В., Аксенова Н.Н., Газатова Н.Д., Затолокин П.А. Особенности клеточного иммунитета и цитокинового репертуара у пациентов с метаболическим синдромом // Бюллетень сибирской медицины, 2012. № 3. С. 53-57. [Litvinova L.S., Kiriyenkova Ye.V., Aksyonova N.N., Gazatova N.D., Zatolokin P.A. Features of cellular immunity and cytokine repertoire in patients with metabolic syndrome. Byulleten` sibirskoy meditsiny = Bulletin of Siberian Medicine, 2012, no. 3, pp. 53-57. (In Russ.)]</mixed-citation><mixed-citation xml:lang="en">Литвинова Л.С., Кириенкова Е.В., Аксенова Н.Н., Газатова Н.Д., Затолокин П.А. Особенности клеточного иммунитета и цитокинового репертуара у пациентов с метаболическим синдромом // Бюллетень сибирской медицины, 2012. № 3. С. 53-57. [Litvinova L.S., Kiriyenkova Ye.V., Aksyonova N.N., Gazatova N.D., Zatolokin P.A. Features of cellular immunity and cytokine repertoire in patients with metabolic syndrome. Byulleten` sibirskoy meditsiny = Bulletin of Siberian Medicine, 2012, no. 3, pp. 53-57. (In Russ.)]</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Невзорова В.А., Помогалова О.Г., Настрадин О.В. Роль эндотелиальной дисфункции в прогрессировании метаболического синдрома от факторов риска до сосудистых катастроф // Тихоокеанский медицинский журнал, 2008. № 3. С. 69-74. [Nevzorova V.A., Pomogalova O.G., Nastradin O.V. The role of endothelial dysfunctions in progressing of the metabolic syndrome from risk factors to vascular disease. Tikhookeanskiy meditsinskiy zhurnal = Pacific Medical Journal, 2008, no. 3, pp. 69-74. (In Russ.)]</mixed-citation><mixed-citation xml:lang="en">Невзорова В.А., Помогалова О.Г., Настрадин О.В. Роль эндотелиальной дисфункции в прогрессировании метаболического синдрома от факторов риска до сосудистых катастроф // Тихоокеанский медицинский журнал, 2008. № 3. С. 69-74. [Nevzorova V.A., Pomogalova O.G., Nastradin O.V. The role of endothelial dysfunctions in progressing of the metabolic syndrome from risk factors to vascular disease. Tikhookeanskiy meditsinskiy zhurnal = Pacific Medical Journal, 2008, no. 3, pp. 69-74. (In Russ.)]</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Cinti S.Transdifferentiation properties of adipocytes in the adipose organ. Am. J. Physiol. Endocrinol. Metab., 2009, Vol. 297, no. 5, pp. 977-986.</mixed-citation><mixed-citation xml:lang="en">Cinti S.Transdifferentiation properties of adipocytes in the adipose organ. Am. J. Physiol. Endocrinol. Metab., 2009, Vol. 297, no. 5, pp. 977-986.</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Gustafson B., Gogg S., Hedjazifar S., Jenndahl L., Hammarstedt A., Smith U. Inflammation and impaired adipogenesis in hypertrophic obesity in man. Am. J. Physiol. Endocrinol. Metab., 2009, Vol. 297, no. 5, pp. 999-1003.</mixed-citation><mixed-citation xml:lang="en">Gustafson B., Gogg S., Hedjazifar S., Jenndahl L., Hammarstedt A., Smith U. Inflammation and impaired adipogenesis in hypertrophic obesity in man. Am. J. Physiol. Endocrinol. Metab., 2009, Vol. 297, no. 5, pp. 999-1003.</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Kang H.S., Okamoto K., Takeda Y., Beak J.Y., Gerrish K., Bortner C.D., DeGraff L.M., Wada T., Xie W., Jetten A.M. Transcriptional profiling reveals a role for RORα in regulating gene expression in obesity-associated inflammation and hepatic steatosis. Physiol. Genomics, 2011, Vol. 43, pp. 818-828.</mixed-citation><mixed-citation xml:lang="en">Kang H.S., Okamoto K., Takeda Y., Beak J.Y., Gerrish K., Bortner C.D., DeGraff L.M., Wada T., Xie W., Jetten A.M. Transcriptional profiling reveals a role for RORα in regulating gene expression in obesity-associated inflammation and hepatic steatosis. Physiol. Genomics, 2011, Vol. 43, pp. 818-828.</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Leibowitz A., Rehman A., Paradis P., Schiffrin E.L. Role of T regulatory lymphocytes in the pathogenesis of high-fructose diet-induced metabolic syndrome. Hypertension, 2013, Vol. 61, pp. 1316-1321.</mixed-citation><mixed-citation xml:lang="en">Leibowitz A., Rehman A., Paradis P., Schiffrin E.L. Role of T regulatory lymphocytes in the pathogenesis of high-fructose diet-induced metabolic syndrome. Hypertension, 2013, Vol. 61, pp. 1316-1321.</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Martín-Cordero L., García J.J., Hinchado M.D., Ortega E. The interleukin-6 and noradrenaline mediated inflammation-stress feedback mechanism is dysregulated in metabolic syndrome: effect of exercise. Cardiovasc. Diabetol., 2011, Vol. 10, no. 12.</mixed-citation><mixed-citation xml:lang="en">Martín-Cordero L., García J.J., Hinchado M.D., Ortega E. The interleukin-6 and noradrenaline mediated inflammation-stress feedback mechanism is dysregulated in metabolic syndrome: effect of exercise. Cardiovasc. Diabetol., 2011, Vol. 10, no. 12.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Picchi A., Gao X., Belmadani S., Potter B.J., Focardi M., Chilian W.M., Zhang C. Tumor necrosis factor-α induces endothelial dysfunction in the prediabetic metabolic syndrome. Circ. Res., 2006, Vol. 99, pp. 69-77.</mixed-citation><mixed-citation xml:lang="en">Picchi A., Gao X., Belmadani S., Potter B.J., Focardi M., Chilian W.M., Zhang C. Tumor necrosis factor-α induces endothelial dysfunction in the prediabetic metabolic syndrome. Circ. Res., 2006, Vol. 99, pp. 69-77.</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Sanada K., Iemitsu M., Murakami H., Tabata I., Yamamoto K., GandoY., Suzuki K., Higuchi M., Miyachi M. PPARγ2 C1431T genotype increases metabolic syndrome risk in young men with low cardiorespiratory fitness. Physiol. Genomics, 2011, Vol. 43, pp. 103-109.</mixed-citation><mixed-citation xml:lang="en">Sanada K., Iemitsu M., Murakami H., Tabata I., Yamamoto K., GandoY., Suzuki K., Higuchi M., Miyachi M. PPARγ2 C1431T genotype increases metabolic syndrome risk in young men with low cardiorespiratory fitness. Physiol. Genomics, 2011, Vol. 43, pp. 103-109.</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Suganami T., Nishida J., Ogawa Y. A paracrine loop between adipocytes and macrophages aggravates inflammatory changes role of free fatty acids and tumor necrosis factor-α. Arterioscler. Thromb. Vasc. Biol., 2005, Vol. 25, pp. 2062-2068.</mixed-citation><mixed-citation xml:lang="en">Suganami T., Nishida J., Ogawa Y. A paracrine loop between adipocytes and macrophages aggravates inflammatory changes role of free fatty acids and tumor necrosis factor-α. Arterioscler. Thromb. Vasc. Biol., 2005, Vol. 25, pp. 2062-2068.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Tesauro M., Schinzari F., Iantorno M., Rizza S., Melina D., Lauro D., Cardillo C. Ghrelin improves endothelial function in patients with metabolic syndrome. Circulation, 2005, Vol. 112, pp. 2986-2992.</mixed-citation><mixed-citation xml:lang="en">Tesauro M., Schinzari F., Iantorno M., Rizza S., Melina D., Lauro D., Cardillo C. Ghrelin improves endothelial function in patients with metabolic syndrome. Circulation, 2005, Vol. 112, pp. 2986-2992.</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Westcott D.J., Del Proposto J.B., Geletka L.M., Wang T., Singer K., Saltiel A.R., Lumeng C.N. MGL1 promotes adipose tissue inflammation and insulin resistance by regulating 7/4hi monocytes in obesity. J. Exp. Med., 2009, Vol. 206, no. 13, pp. 3143-3156.</mixed-citation><mixed-citation xml:lang="en">Westcott D.J., Del Proposto J.B., Geletka L.M., Wang T., Singer K., Saltiel A.R., Lumeng C.N. MGL1 promotes adipose tissue inflammation and insulin resistance by regulating 7/4hi monocytes in obesity. J. Exp. Med., 2009, Vol. 206, no. 13, pp. 3143-3156.</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
