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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="other" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Journal of microbiology, epidemiology and immunobiology</journal-id><journal-title-group><journal-title xml:lang="en">Journal of microbiology, epidemiology and immunobiology</journal-title><trans-title-group xml:lang="ru"><trans-title>Журнал микробиологии, эпидемиологии и иммунобиологии</trans-title></trans-title-group></journal-title-group><issn publication-format="print">0372-9311</issn><issn publication-format="electronic">2686-7613</issn><publisher><publisher-name xml:lang="en">Central Research Institute for Epidemiology</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">13680</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></subject></subj-group></article-categories><title-group><article-title xml:lang="en">CHARACTERISTIC OF EARLY MUCOSAL IMMUNE RESPONSE IN MICE DURING INTRAVAGINAL INFECTION CAUSED BY CHLAMYDIA MURIDARUM</article-title><trans-title-group xml:lang="ru"><trans-title>ХАРАКТЕРИСТИКА РАННЕГО МУКОЗАЛЬНОГО ИММУННОГО ОТВЕТА У МЫШЕЙ ПРИ ИНТРАВАГИНАЛЬНОЙ ИНФЕКЦИИ, ВЫЗВАННОЙ CHLAMYDIA MURIDARUM</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Kobets</surname><given-names>N V</given-names></name><name xml:lang="ru"><surname>Кобец</surname><given-names>Н В</given-names></name></name-alternatives><bio xml:lang="ru"><p>НИИ эпидемиологии и микробиологии им. Н.Ф.Гамалеи, Москва</p></bio><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Koroleva</surname><given-names>E A</given-names></name><name xml:lang="ru"><surname>Королева</surname><given-names>Е А</given-names></name></name-alternatives><bio xml:lang="ru"><p>НИИ эпидемиологии и микробиологии им. Н.Ф.Гамалеи, Москва</p></bio><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Zigangirova</surname><given-names>N A</given-names></name><name xml:lang="ru"><surname>Зигангирова</surname><given-names>Н А</given-names></name></name-alternatives><bio xml:lang="ru"><p>НИИ эпидемиологии и микробиологии им. Н.Ф.Гамалеи, Москва</p></bio><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en"></institution></aff><aff><institution xml:lang="ru">НИИ эпидемиологии и микробиологии им. Н.Ф.Гамалеи, Москва</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2012-08-15" publication-format="electronic"><day>15</day><month>08</month><year>2012</year></pub-date><volume>89</volume><issue>4</issue><issue-title xml:lang="en">NO4 (2012)</issue-title><issue-title xml:lang="ru">№4 (2012)</issue-title><fpage>20</fpage><lpage>26</lpage><history><date date-type="received" iso-8601-date="2023-06-09"><day>09</day><month>06</month><year>2023</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2012, Kobets N.V., Koroleva E.A., Zigangirova N.A.</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2012, Кобец Н.В., Королева Е.А., Зигангирова Н.А.</copyright-statement><copyright-year>2012</copyright-year><copyright-holder xml:lang="en">Kobets N.V., Koroleva E.A., Zigangirova N.A.</copyright-holder><copyright-holder xml:lang="ru">Кобец Н.В., Королева Е.А., Зигангирова Н.А.</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">https://creativecommons.org/licenses/by/4.0</ali:license_ref></license></permissions><self-uri xlink:href="https://microbiol.crie.ru/jour/article/view/13680">https://microbiol.crie.ru/jour/article/view/13680</self-uri><abstract xml:lang="en"><p>Aim. Comparison of features of recruitment to infection focus of cells mediating early immune
reactions in intravaginally infected mice that had previously received or not received covinan
(progesterone analogue). Materials and methods. A/Sn and BALB/c line mice were used in the
study. C. muridarum strain Nigg infection was carried out intravaginally or intraperitoneally. For
synchronization of sexual cycle a group of mice received subcutaneously a synthetic analogue of
progesterone - proligeston (covinan) at a single dose of 33 mg/kg. Acute urogenital infection was
evaluated by culture method. Quantitative determination of C. muridarum DNA (including study
of persistence) was carried out by real time PCR. Subpopulation structure of cell population of
peritoneal and vaginal lavage was evaluated by flow cytofluorometry. Results. Intravaginal infection
of mice that had not received covinan resulted in a pronounced recruitment of cells into vaginal
cavity at 24 hours after the infection. Influx of neutrophils, dendritic cells and T-lymphocytes was
especially pronounced. Prior administration of covinan practically nullified cell recruitment to
infection focus though partial preservation of subpopulations of activated dendritic cells and CD8+
T-cells was observed. Conclusion. In mice with artificially induced by progesterone sensitivity to
chlamydias the ability of recruitment to the infection focus of cells that mediate early immune
reactions is reduced, that gives evidence on the importance of these reactions for infection outcome.</p></abstract><trans-abstract xml:lang="ru"><p>Цель. Сравнение особенностей рекрутирования клеток, опосредующих ранние иммун-
ные реакции, к очагу инфекции у интравагинально зараженных мышей, предварительно
получавших или не получавших ковинан (аналог прогестерона). Материалы и методы. В
работе использовали мышей линий A/Sn и BALB/c. Заражение C. muridarum штамм Nigg
проводили интравагинально или внутрибрюшинно. Для синхронизации полового цикла
группе мышей вводили подкожно синтетический аналог прогестерона - пролигестон
(ковинан) в дозе 33 мг/кг однократно. Острую урогенитальную инфекцию оценивали
культуральным методом. Количественное определение ДНК C. muridarum (в том числе
для изучения персистенции) проводили методом Real-time PCR. Субпопуляционную
структуру клеточных популяций перитонеального и вагинального смыва оценивали ме-
тодом проточной цитофлуориметрии Результаты. Интравагинальное заражение мышей,
не получавших ковинан, приводило к выраженному рекрутированию клеток в вагиналь-
ную полость на 24 ч после заражения. Особенно был выражен приток нейтрофилов,
дендритных клеток и Т-лимфоцитов. Предварительное введение ковинана практически
сводило к нулю рекрутирование клеток к очагу инфекции, хотя и наблюдалась частичная
сохранность субпопуляций активированных дендритных клеток и CD8+ Т клеток.
Заключение. Показано, что у мышей с искусственно индуцированной прогестероном чув-
ствительностью к хламидиям нарушена способность к рекрутированию в очаг заражения
клеток, опосредующих ранние иммунные реакции, что свидетельствует о важности этих
реакций для исхода инфекции.</p></trans-abstract><kwd-group xml:lang="en"><kwd>Chlamydia</kwd><kwd>Chlamydia</kwd><kwd>cytokines</kwd><kwd>intravaginal infection</kwd><kwd>progesteron</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>цитокины</kwd><kwd>интравагинальное заражение</kwd><kwd>прогестерон</kwd></kwd-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Зигангирова Н.А., Федина Е.Д., Зорина В.В. и др. Мишень-направленный поиск антивирулентных лекарственных препаратов. Журн. микробиол. 2009, 4: 71-77.</mixed-citation></ref><ref id="B2"><label>2.</label><mixed-citation>Cengiz T., Aydooanli L., Baykam M. et al. Chlamydial infections and male infertility. Intern. Urol. Nephrol. 1997, 29 (6): 687-693.</mixed-citation></ref><ref id="B3"><label>3.</label><mixed-citation>Darville Т. Chlamydia trachomatis genital infection in adolescents and young adults. Adv. Exper. Med. Biol. 2006, 582: 85-100.</mixed-citation></ref><ref id="B4"><label>4.</label><mixed-citation>Frazer L.C., O'Connell C.M., Andrews C.W. et al. Enhanced neutrophil longevity and recruitment contribute to the severity of oviduct pathology during Chlamydia muridarum infection. Infect. Immun. 2011, 79 (10): 4029-4041.</mixed-citation></ref><ref id="B5"><label>5.</label><mixed-citation>Howie S., Horner P., Horne A. et al. Immunity and vaccines against sexually transmitted Chlamydia trachomatis infection. Curr. Opin. Infect. Dis. 2011, 24 (1): 56-61.</mixed-citation></ref><ref id="B6"><label>6.</label><mixed-citation>Nagarajan U.M., Sikes J., Prantner D. et al. MyD88 deficiency leads to decreased NK cell gamma interferon production and T cell recruitment during Chlamydia muridarum genital tract infection, but a predominant Th1 response and enhanced monocytic inflammation are associated with infection resolution. Infect. Immun. 2011, 79 (1): 486-498.</mixed-citation></ref><ref id="B7"><label>7.</label><mixed-citation>Murthy A.K., Li W., Chaganty B.K. et al. Tumor necrosis factor alpha production from CD8+ T cells mediates oviduct pathological sequelae following primary genital Chlamy dia muridarum infection. Infect. Immun. 2011, 79 (7): 2928-2935.</mixed-citation></ref><ref id="B8"><label>8.</label><mixed-citation>Scurlock A.M., Frazer L.C., Andrews C.W. Jr. et al. Interleukin-17 contributes to generation of Th1 immunity and neutrophil recruitment during Chlamydia muridarum genital tract infection but is not required for macrophage influx or normal resolution of infection. Infect. Immun. 2011, 79 (3): 1349-1362.</mixed-citation></ref><ref id="B9"><label>9.</label><mixed-citation>Wyrick P.B. Chlamydia trachomatis per sistence in vitro: an overview. J. Infect. Dis. 2010, 201 (2): S88-S95.</mixed-citation></ref><ref id="B10"><label>10.</label><mixed-citation>Xiao Y., Zhong Y., Su H. et al. NF-kappa B activation is not required for Chlamydia trachomatis inhibition of host epithelial cell apoptosis. J. Immunol. 2005, 174 (3): 1701-1708.</mixed-citation></ref></ref-list></back></article>
