<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE root>
<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">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">14207</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">SIGNS OF MICROBIAL SENSIBILIZATION IN PATIENTS WITH VARIOUS CARDIOVASCULAR DISEASES</article-title><trans-title-group xml:lang="ru"><trans-title>ПРИЗНАКИ МИКРОБНОЙ СЕНСИБИЛИЗАЦИИ У БОЛЬНЫХ С РАЗЛИЧНЫМИ СЕРДЕЧНО-СОСУДИСТЫМИ ЗАБОЛЕВАНИЯМИ</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Karpunina</surname><given-names>N. S</given-names></name><name xml:lang="ru"><surname>Карпунина</surname><given-names>Н. С</given-names></name></name-alternatives><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Bakhmetiev</surname><given-names>B. A</given-names></name><name xml:lang="ru"><surname>Бахметьев</surname><given-names>Б. А</given-names></name></name-alternatives><xref ref-type="aff" rid="aff2"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Zaikina</surname><given-names>M. V.</given-names></name><name xml:lang="ru"><surname>Заикина</surname><given-names>М. В</given-names></name></name-alternatives><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">Perm State Medical Academy</institution></aff><aff><institution xml:lang="ru">Пермская государственная медицинская академия</institution></aff></aff-alternatives><aff-alternatives id="aff2"><aff><institution xml:lang="en">Research Institute of Ecology and Genetics of Microorganisms</institution></aff><aff><institution xml:lang="ru">Институт экологии и генетики микроорганизмов</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2015-02-15" publication-format="electronic"><day>15</day><month>02</month><year>2015</year></pub-date><volume>92</volume><issue>1</issue><issue-title xml:lang="en">NO1 (2015)</issue-title><issue-title xml:lang="ru"/><fpage>75</fpage><lpage>81</lpage><history><date date-type="received" iso-8601-date="2023-06-13"><day>13</day><month>06</month><year>2023</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2015, Karpunina N.S., Bakhmetiev B.A., Zaikina M.V.</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2015, Карпунина Н.С., Бахметьев Б.А., Заикина М.В.</copyright-statement><copyright-year>2015</copyright-year><copyright-holder xml:lang="en">Karpunina N.S., Bakhmetiev B.A., Zaikina M.V.</copyright-holder><copyright-holder xml:lang="ru">Карпунина Н.С., Бахметьев Б.А., Заикина М.В.</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/14207">https://microbiol.crie.ru/jour/article/view/14207</self-uri><abstract xml:lang="en"><p>Aim. Analysis of intensity of non-specific (level of sera cytokines) and specific (titers of antibodies against Chlamydophila pneumoniae) factors of humoral immunity in patients with arterial hypertension and various forms of ischemic heart diseases. Materials and methods. 282 individuals were the object of examination - 157 (55.7%) males. 8 groups were formed, comparable by age: 1 - 32 individuals with exertional angina pectoris of the III functional class; 2 - 20 individuals with healing Q-positive myocardial infarction (MI); 3 - 15 individuals with Q-negative healing MI; 4 - 15 individuals with unstable angina pectoris; 5 - 40 individuals with persisting atrium fibrillation; 6 - 35 individuals with clinically significant chronic heart failure; 7 - 92 patients with hypertension of the II stage; 33 conditionally healthy composed the control group. Class A and G immunoglobulins against C. pneumoniae, IL-ф, -6, -17, TNFa content in blood were determined. Results. The proportion of seropositive individuals in groups with IgG and IgA titer characteristics was determined. Data on the level of cytokines, taking into the account seropositivity, and titer increase are presented. Correlations between hemostasis system were established, that demonstrate increase of thrombophilia in the presence of persistent infection, mediated via induction of cytokine production. Significant differences by instrumental parameters depending on seropositivity were not obtained. Conclusion. Contribution of microbial sensibilization and latent inflammation in the development and destabilization of atherogenesis-associated diseases seems evident.</p></abstract><trans-abstract xml:lang="ru"><p>Цель. Анализ выраженности неспецифических (уровень сывороточных цитокинов) и специфических (титры антител к Chlamydophila pneumoniae) факторов гуморального иммунитета у больных артериальной гипертензией и различными формами ишемической болезни сердца. Материалы и методы. Объектом наблюдений были 282 человека, мужчин - 157 (55,7%). Сформировано 8 групп, сопоставимых по возрасту: 1 - 32 человека со стенокардией напряжения III функционального класса; 2 - 20 человек с заживающим Q-позитивным инфарктом миокарда (ИМ); 3 - 15 человек с Q-негативным заживающим ИМ; 4 - 15 человек с нестабильной стенокардией; 5 - 40 человек с персистирующей фибрилляцией предсердий; 6 - 35 пациентов с клинически значимой хронической сердечной недостаточностью; 7 - 92 пациента с гипертонической болезнью II стадии; контрольную группу составили 33 условно здоровых пациента. Определяли иммуноглобулины к C.pneumoniae классов А и G, содержание ИЛ-1 в, -6, -17, ФНО-а в крови. Результаты. Определена доля серопозитивных лиц в группах с характеристикой титра IgG и IgA. Представлены данные по уровню цитокинов с учетом серопозитивности и нарастания титра. Установлены корреляции с показателями системы гемостаза, демонстрирующие нарастание тромбофилии в присутствии персистирующей инфекции, опосредованно, через индукцию выработки цитокинов. Значимых отличий по инструментальным параметрам в зависимости от серопозитивности не получено. Заключение. Вклад микробной сенсибилизации и латентного воспаления в развитие и дестабилизацию атерогенез-ассоциированных заболеваний представляется очевидным.</p></trans-abstract><kwd-group xml:lang="en"><kwd>sera cytokines</kwd><kwd>cardiovascular diseases</kwd><kwd>antibodies against Chlamydophila pneumoniae</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>сывороточные цитокины</kwd><kwd>сердечно-сосудистые заболевания</kwd><kwd>антитела к Chlamydophila pneumoniae</kwd></kwd-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Шапошникова А.И. Хламидийная инфекция и показатели воспаления при фибрилляции предсердий у больных ишемической болезнью сердца, их прогностическая значимость. Автореф. дис. канд. мед. наук. Пермь, 2005.</mixed-citation></ref><ref id="B2"><label>2.</label><mixed-citation>Corrales-Medina V.F., Madjid M., Musher D.M. Role of acute infection in triggering acute coronary syndromes. Lancet Infect. Dis. 2010, 10 (2): 83-92.</mixed-citation></ref><ref id="B3"><label>3.</label><mixed-citation>Elkind M.S. Infectious burden: a new risk factor and treatment target for atherosclerosis. Infect. Disord. Drug. Targets. 2010, 10 (2): 84-90.</mixed-citation></ref><ref id="B4"><label>4.</label><mixed-citation>Epstein S.E., Zhu J., Najafi A.H. Insights into the role of infection in atherogenesis and in plaque rupture. Circulation. 2009, 119 (24): 3133-3141.</mixed-citation></ref><ref id="B5"><label>5.</label><mixed-citation>Fong I.W New perspectives of infections in cardiovascular disease. Curr. Cardiol. Rev. 2009, 5 (2): 87-104.</mixed-citation></ref><ref id="B6"><label>6.</label><mixed-citation>Honarmand H. Atherosclerosis induced by Chlamydophila pneumoniae: a controversial theory. interdisciplinary perspectives on infectious diseases. 2013, Article ID 941392, 11 pages.</mixed-citation></ref><ref id="B7"><label>7.</label><mixed-citation>Kreutmayer S., Csordas A., Kern J. et al. Chlamydia pneumoniae infection acts as an endothelial stressor with the potential to initiate the earliest heat shock protein 60-dependent inflammatory stage of atherosclerosis. Cell. Stress Chaperones. 2013, 18: 259-268.</mixed-citation></ref><ref id="B8"><label>8.</label><mixed-citation>Madjid M., Vfela D., Khalili-Tabrizi H. Systemic infections cause exaggerated local inflammation in atherosclerotic coronary arteries: clues to the triggering effect of acute infections on acute coronary syndromes. Tex. Heart. Inst. J. 2007, 34 (1): 11-18.</mixed-citation></ref><ref id="B9"><label>9.</label><mixed-citation>Pietro M., Filardo S., Santis F. et al. Chlamydia pneumoniae infection in atherosclerotic lesion development through oxidative stress: a brief overview. Int. J. Mol. Sci. 2013, 14: 1510515120.</mixed-citation></ref><ref id="B10"><label>10.</label><mixed-citation>Shah PK. Link between infection and atherosclerosis: who are the culprits: viruses, bacteria, both, or neither? Circulation. 2001, 103 (1): 5-6.</mixed-citation></ref><ref id="B11"><label>11.</label><mixed-citation>Simanek A.M., Dowd J.B., Aiello A. Persistent pathogens linking socioeconomic position and cardiovascular disease in the US. Int. J. Epidemiol. 2009, 38 (3): 775-787.</mixed-citation></ref><ref id="B12"><label>12.</label><mixed-citation>Steptoe A., Shamaei-Tousi A., Gylfe A. Socioeconomic status, pathogen burden and cardiovascular disease risk. Heart. 2007, 93 (12): 1567-1570.</mixed-citation></ref><ref id="B13"><label>13.</label><mixed-citation>Wang Ch.-M., Kaltenboeck B. Exacerbation of chronic inflammatory diseases by infectious agents: fact or fiction? World J. Diabetes. 2010, 1 (2): 27-35.</mixed-citation></ref><ref id="B14"><label>14.</label><mixed-citation>Wildgruber M., Swirski F.K., Zernecke A. Molecular imaging of inflammation in atherosclerosis. Theranostics. 2013, 11: 865-884.</mixed-citation></ref></ref-list></back></article>
