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<article 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" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="research-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Epidemiology and Infectious Diseases</journal-id><journal-title-group><journal-title xml:lang="en">Epidemiology and Infectious Diseases</journal-title><trans-title-group xml:lang="ru"><trans-title>Эпидемиология и инфекционные болезни</trans-title></trans-title-group></journal-title-group><issn publication-format="print">3034-2007</issn><issn publication-format="electronic">3034-2015</issn><publisher><publisher-name xml:lang="en">Eco-Vector</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">40811</article-id><article-id pub-id-type="doi">10.17816/EID40811</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Articles</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Статьи</subject></subj-group><subj-group subj-group-type="article-type"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">Immunopathogenetic features of bacterial purulent meningitides</article-title><trans-title-group xml:lang="ru"><trans-title>Иммунопатогенетические особенности бактериальных гнойных менингитов</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Balmasova</surname><given-names>I. P</given-names></name><name xml:lang="ru"><surname>Балмасова</surname><given-names>Ирина Петровна</given-names></name></name-alternatives><bio xml:lang="ru"><p>доктор мед. наук, проф., зав. лаб. патогенеза и методов лечения инфекционных заболеваний Научно-исследовательского медико-стоматологического института</p></bio><email>iri.balm@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Vengerov</surname><given-names>Yu. Ya</given-names></name><name xml:lang="ru"><surname>Венгеров</surname><given-names>Юрий Яковлевич</given-names></name></name-alternatives><bio xml:lang="ru"><p>доктор мед. наук, профессор, проф., каф. инфекционных болезней и эпидемиологии</p></bio><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Razdobarina</surname><given-names>S. E</given-names></name><name xml:lang="ru"><surname>Раздобарина</surname><given-names>Светлана Евгеньевна</given-names></name></name-alternatives><bio xml:lang="ru"><p>аспирант каф. инфекционных болезней и эпидемиологии</p></bio><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Nagibina</surname><given-names>M. V</given-names></name><name xml:lang="ru"><surname>Нагибина</surname><given-names>Маргарита Васильевна</given-names></name></name-alternatives><bio xml:lang="ru"><p>канд. мед. наук, доцент каф. инфекционных болезней и эпидемиологии</p></bio><email>infektor03@gmail.com</email><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">Moscow State University of Medicine and Dentistry named after A.I. Evdokimov</institution></aff><aff><institution xml:lang="ru">ГБОУ ВПО «Московский государственный медико-стоматологический университет им. А.И. Евдокимова» Минздрава России</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2014-10-15" publication-format="electronic"><day>15</day><month>10</month><year>2014</year></pub-date><volume>19</volume><issue>5</issue><issue-title xml:lang="en">VOL 19, NO5 (2014)</issue-title><issue-title xml:lang="ru">ТОМ 19, №5 (2014)</issue-title><fpage>4</fpage><lpage>9</lpage><history><date date-type="received" iso-8601-date="2020-07-23"><day>23</day><month>07</month><year>2020</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2014, Eco-vector</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2014, ООО "Эко-вектор"</copyright-statement><copyright-year>2014</copyright-year><copyright-holder xml:lang="en">Eco-vector</copyright-holder><copyright-holder xml:lang="ru">ООО "Эко-вектор"</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/></permissions><self-uri xlink:href="https://rjeid.com/1560-9529/article/view/40811">https://rjeid.com/1560-9529/article/view/40811</self-uri><abstract xml:lang="en"><p>The aim of the study. Comparative assessment of the state of cells of the immune system in patients with purulent bacterial meningitides caused by N.meningitidis and S.pneumoniae . Materials and methods. By the method offlow cytofluorometry there were tested blood and cerebrospinal fluid of 65 patients with bacterial purulent meningitis, with the meningococcal (38 people) and pneumococcal (27 people) nature of the disease. Results. There were revealed general consistencies of the immune response to CNS infection with meningococcus andpneumococcus: the fall of the number of CD16+ CD56+(NK) and the gain in the number of CD19+ cells in the blood, an increase in the absolute number of T lymphocytes, especially, CD3+ CD8+ and NK. In pneumococcal meningitis there was noted the more pronounced upsurge in the absolute number of the NKT (CD3+CD56+) and B-lymphocytes in the blood whereas in cerebrospinal fluid - the more pronounced upturn in the absolute number of NKT that testified to the severe course of the disease. Conclusion. As a result of performed studies there was identified a series of consistencies for the development of the immune response in bacterial purulent meningitides of meningococcal and pneumococcal etiology, which show the high informativeness of the study of immunograms of cerebrospinal fluid in these diseases as compared with blood. In the latter case, immunological studies may contribute not only to the identification of general consistencies of the development of the immune response in bacterial meningitis, but also serve as a basis for the differentiation of the impact of meningococcal and pneumococcal infection on immunocompetent cells, as well as to reflect the severity of the course of the disease, affecting the nature of the therapy.</p></abstract><trans-abstract xml:lang="ru"><p>Цель исследования - сравнительная оценка состояния клеток иммунной системы у больных бактериальными гнойными менингитами, вызванными N.meningitidis и S.pneumoniae. Материалы и методы. Методом проточной цитофлуориметрии были тестированы кровь и спинномозговая жидкость 65 больных бактериальными гнойными менингитами с менингококковой (38 человек) и пневмококковой (27 человек) природой заболевания. Результаты. Были выявлены общие закономерности иммунного ответа на инфицирование ЦНС менингококком и пневмококком: падение числа CD16+CD56+ (естественных киллеров - ЕК) и рост числа CD19+-клеток в крови, рост абсолютного числа Т-лимфоцитов, особенно CD3+CD8+, и ЕК. При пневмококковом менингите отмечен более выраженный рост абсолютного числа ЕКТ (CD3+CD56+) и В-лимфоцитов в крови, а в спинномозговой жидкости более выраженный рост абсолютного числа ЕКТ свидетельствовал о тяжелом течении заболевания. Заключение. В результате проведенных исследований был выявлен ряд закономерностей развития иммунного ответа при бактериальных гнойных менингитах менингококковой и пневмококковой этиологии, которые показывают большую информативность исследования иммунограмм спинномозговой жидкости при данных заболеваниях по сравнению с кровью. В последнем случае иммунологические исследования могут не только способствовать выявлению общих закономерностей развития иммунного ответа при бактериальных менингитах, но и служить основой для дифференциации воздействия менингококка и пневмококка на иммунокомпетентные клетки, а также отражать тяжесть течения заболевания, влияя на характер проводимой терапии.</p></trans-abstract><kwd-group xml:lang="en"><kwd>bacterial purulent meningitides</kwd><kwd>pneumococcal</kwd><kwd>meningococcal disease</kwd><kwd>the immune response</kwd><kwd>lymphocytes</kwd><kwd>NKT</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>бактериальные гнойные менингиты</kwd><kwd>пневмококк</kwd><kwd>менингококк</kwd><kwd>иммунный ответ</kwd><kwd>лимфоциты</kwd><kwd>ЕКТ</kwd></kwd-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Венгеров Ю.Я, Ченцов В.Б., Нагибина М.В. и др. Современные принципы диагностики и лечения больных бактериальными гнойными менингитами. Consilium Medicum 2010; 12: 54-67.</mixed-citation></ref><ref id="B2"><label>2.</label><mixed-citation>Воробьев А.В., Быков А.С., Пашков Е.П., Рыбакова А.М. Микробиология. M.: Медицина; 2003.</mixed-citation></ref><ref id="B3"><label>3.</label><mixed-citation>Королева И.С., Белошицкий И.С., Королева М.А. и др. Менингококковая инфекция и гнойные бактериальные менингиты в Российской Федерации: десятилетнее эпидемиологическое наблюдение. Эпидемиология и инфекционные болезни. Актуальные вопросы. 2013; 2: 15-20.</mixed-citation></ref><ref id="B4"><label>4.</label><mixed-citation>Королева И.С., Белошицкий И.С., Чистякова Г.Г., Быкова Р.Н. Эпидемиологический надзор за гнойными бактериальными менингитами. Эпидемиология и инфекционные болезни. 2004; 3: 21-5.</mixed-citation></ref><ref id="B5"><label>5.</label><mixed-citation>Пилипенко В.В. Бактериальные гнойные менингиты - исторический экскурс. Вестник Российской военно-медицинской академии. 2011; 1: 266-72.</mixed-citation></ref><ref id="B6"><label>6.</label><mixed-citation>Сепиашвили Р.И., Балмасова И.П. Физиологические основы функционирования новой субпопуляции лимфоцитов - ЕКТ. Аллергология и иммунология. 2005. 6 (1): 14-22.</mixed-citation></ref><ref id="B7"><label>7.</label><mixed-citation>Ali F., Lee M.E., Iannelli F. et al. Streptococcus pneumoniae associated human macrophage apoptosis after bacterial internalization via complement and Fcgamma receptors correlates with intracellular bacterial load. J. Infect. Dis. 2003; 188 (8): 1119-31.</mixed-citation></ref><ref id="B8"><label>8.</label><mixed-citation>Arjunaraja S., Paoletti L.C., Snapper C.M. Structurally identical capsular polysaccharide expressed by intact Group B Streptococcus versus Streptococcus pneumoniae elicits distinct murine polysaccharide-specific IgG responses in vivo. J Immunol. 2012; 188 (11): 5238-46.</mixed-citation></ref><ref id="B9"><label>9.</label><mixed-citation>Brandl C., Ortler S., Herrmann T. et al. B7-H1-deficiency enhances the potential of tolerogenic dendritic cells by activating CD1d-restricted type II NKT cells. PLoS One. 2010; 5 (5): e10800.</mixed-citation></ref><ref id="B10"><label>10.</label><mixed-citation>Brouwer M.C., van de Beek D. Bacterial meningitis. Ned. Tijdschr. Tandheelkd. 2012; 119 (5): 238-242.</mixed-citation></ref><ref id="B11"><label>11.</label><mixed-citation>Edmon K., Clark A., Korczak V.S. et al. Global and regional risk of disabling sequelae from bacterial meningitis: a systematic review and meta-analysis. Lancet Infect. Dis. 2010; 10 (5): 317-28.</mixed-citation></ref><ref id="B12"><label>12.</label><mixed-citation>Foster R.A., Carlring J., Lees A. et al. Functional T-cell deficiency in adolescents who experience serogroup C meningococcal disease despite receiving the meningococcal serogroup C conjugate vaccine. Clin. Vaccine. Immunol. 2010; 17(7): 1104-10.</mixed-citation></ref><ref id="B13"><label>13.</label><mixed-citation>Hammerschmidt S., Bethe G., Remane P.H., Chhatwal G.S.: Identification of pneumococcal surface protein A as a lactoferrinbinding protein of Streptococcus pneumoniae. Infect. and Immun. 1999; 67 (4): 1683-7.</mixed-citation></ref><ref id="B14"><label>14.</label><mixed-citation>Holley M.M., Kielian T. Th1 and Th17 cells regulate innate immune responses and bacterial clearance during central nervous system infection. J. Immunol. 2012; 188 (3): 1360-70.</mixed-citation></ref><ref id="B15"><label>15.</label><mixed-citation>Hyams C., Camberlein E., Cohen J.M. et al. The Streptococcus pneumoniae capsule inhibits complement activity and neutrophil phagocytosis by multiple mechanisms. Infect. and Immun. 2010; 78 (2): 704-15.</mixed-citation></ref><ref id="B16"><label>16.</label><mixed-citation>Jafri R.Z., Ali A., Messonnier N.E. et al. Global epidemiology of invasive meningococcal disease. Populat. Hlth Metrics. 2013; 11 (1): 17-26.</mixed-citation></ref><ref id="B17"><label>17.</label><mixed-citation>Lertmemongkolchai G., Cai G., Hunter C.A., Bancroft G.J. Bystander activation of CD8+ T-cells contributes to the rapid production of IFNy in response to bacterial pathogens. J. Immunol. 2001; 166 (2): 1097-105.</mixed-citation></ref><ref id="B18"><label>18.</label><mixed-citation>Mukerji R., Mirza S., Roche A.M. et al. Pneumococcal surface protein A inhibits complement deposition on the pneumococcal surface by competing with the binding of C-reactive protein to cell-surface phosphocholine. J. Immunol. 2012; 189 (11): 5327-35.</mixed-citation></ref><ref id="B19"><label>19.</label><mixed-citation>Oh S.J., Chung D.H. Invariant NKT cells producing IL-4 or IL-10, but not IFN-gamma, inhibit the Th1 response in experimental autoimmune encephalomyelitis, whereas none of these cells inhibits the Th17 response. J. Immunol. 2011; 186 (12): 6815-21.</mixed-citation></ref><ref id="B20"><label>20.</label><mixed-citation>Parekh V.V., Wu L., Olivares-Villagomez D. et al. Activated invariant NKT cells control central nervous system autoimmunity in a mechanism that involves myeloid-derived suppressor cells. J. Immunol. 2013; 190 (5): 1948-60.</mixed-citation></ref><ref id="B21"><label>21.</label><mixed-citation>Pollard A.J., Galassini R., van der Voort E.M.R. et al. Cellular immune responses to Neisseria meningitidis in children. Infect. and Immun. 1999; 67 (5): 2452-63.</mixed-citation></ref><ref id="B22"><label>22.</label><mixed-citation>Pomar V., Benito N., Lopez-Contreras J. et al. Spontaneous gram-negative bacillary meningitis in adult patients: characteristics and outcome. BMC Infect. Dis. 2013; 13 (1): 451-62.</mixed-citation></ref><ref id="B23"><label>23.</label><mixed-citation>Ricci S., Gerlini A., Pammolli A. et al. Contribution of different pneumococcal virulence factors to experimental meningitis in mice. BMC Infect. Dis. 2013; 13 (1): 444-60.</mixed-citation></ref><ref id="B24"><label>24.</label><mixed-citation>Robinson K., Neal K.R., Howard C. et al. Characterization of humoral and cellular immune responses elicited by meningococcal carriage. Infect. and Immun. 2002; 70 (3): 1301-09.</mixed-citation></ref><ref id="B25"><label>25.</label><mixed-citation>Rock R.B., Gekker G., Hu S. et al. Role of microglia in central nervous system infections. Clin. Microbiol. Rev. 2004; 17 (4): 942-64.</mixed-citation></ref><ref id="B26"><label>26.</label><mixed-citation>Skoczynska A., Wasko I., Kuch A. et al. A decade of invasive meningococcal disease surveillance in poland. PLoS One. 2013; 8 (8): e71943.</mixed-citation></ref><ref id="B27"><label>27.</label><mixed-citation>Tsunoda I., Tanaka T., Fujinami R.S. Regulatory role of CD1d in neurotropic virus infection. J. Virol. 2008; 82 (20): 10279-89.</mixed-citation></ref><ref id="B28"><label>28.</label><mixed-citation>Tu A.H., Fulgham R.L., McCrory M.A. et al. Pneumococcal surface protein A inhibits complement activation by Streptococcus pneumoniae. Infect. and Immun. 1999; 67 (9): 4720-4.</mixed-citation></ref><ref id="B29"><label>29.</label><mixed-citation>Van de Beek D., de Gans J., Tunkel A.R., Wijdicks E.F. Community-acquired bacterial meningitis in adults. N. Enol. J. Med. 2006; 354 (1): 44-53.</mixed-citation></ref></ref-list></back></article>
