Russian Journal of Infection and ImmunityRussian Journal of Infection and ImmunityИнфекция и иммунитет2220-76192313-7398SPb RAACI849110.15789/2220-7619-ASG-8491REVIEWSОБЗОРЫReview ArticleAutoimmune streptococcal glomerulonephritis: the problem of nephritogenicity of Streptococcus pyogenesАутоиммунный стрептококковый гломерулонефрит: проблема нефритогенности Streptococcus pyogeneshttps://orcid.org/0000-0001-7687-23487003982261BurovaLarisa A.БуроваЛариса Александровна
Russian Federation

MD, Dr. Sci. (Med.), Leading Research Associate, Department of Molecular Microbiology

доктор медицинских наук, ведущий научный сотрудник Отдела молекулярной микробиологии

lburova@yandex.ruhttps://orcid.org/0000-0003-2312-55897101829979SuvorovAlexander N.СуворовАлександр Николаевич
Russian Federation

MD, Dr. Sci. (Med.), Professor, Corresponding Member of the Russian Academy of Sciences, Head Department of Molecular Microbiology

доктор медицинских наук, профессор, член-корреспондент РАН, руководитель Отдела молекулярной микробиологии

alexander_suvorov1@hotmail.comhttps://orcid.org/0000-0002-5906-677155404484800PigarevskyPeter V.ПигаревскийПетр Валерьевич
Russian Federation

Dr. Sci. (Biology), Head Department of General Morphology

доктор биологических наук, руководитель Отдела общей морфологии

pigarevsky@mail.ruhttps://orcid.org/0000-0002-3310-92947004990713TotolianArtem A.ТотолянАртем Акопович
Russian Federation

MD, Dr. Sci. (Med.), Professor, Academician RAS, Chief Research Associate, Department of Molecular Microbiology

доктор медицинских наук, профессор, академик РАН, главный научный сотрудник Отдела молекулярной микробиологии

totolyan@hotmail.comInstitute of Experimental MedicineФГБНУ Институт экспериментальной медицины16052023260620231334094292304202307052023Copyright ©; 2023, Burova L.A., Suvorov A.N., Pigarevsky P.V., Totolian A.A.Copyright ©; 2023, Бурова Л.А., Суворов А.Н., Пигаревский П.В., Тотолян А.А.2023Burova L.A., Suvorov A.N., Pigarevsky P.V., Totolian A.A.Бурова Л.А., Суворов А.Н., Пигаревский П.В., Тотолян А.А.https://creativecommons.org/licenses/by/4.0https://iimmun.ru/iimm/article/view/8491

Acute post-streptococcal glomerulonephritis usually occurs as a complication after a streptococcal infection due to untimely or inadequate antibiotic therapy. The etiology of post-streptococcal glomerulonephritis has been studied rather comprehensively. Today, both clinicians and microbiologists do not deny the dominant role of Streptococcus pyogenes (streptococcus attributed to serological group A, GAS). Usually, emergence of acute post-streptococcal glomerulonephritis (APSGN) is associated with the so-called GAS-related "nephritogenicity" often judged by appearance and accumulation of antibodies to the antigens and extracellular products of streptococcal cells in patient blood. This interpretation is quite loose and most likely evidence about a link to the bacterial strain, rather than its nephritogenicity. Many studies refer and still attribute a leading role of "nephritogenic" factors to various streptococcal antigens and related biologically active products. Streptococcal nephritogenic factors include cross-reacting antigens, streptokinase, cysteine proteinase, endostreptosin – a GAS cell membrane protein as well as plasmin-tropic enzyme glyceraldehyde-3-phosphate dehydrogenase. Nephritogenicity of all such streptococcal products is suspected to result from the fact that they are found in renal biopsies like specific patient blood serum antibodies. Regarding a term of nephritogenicity, it has been evidenced that it cannot be attributed to any specific streptococcal cell product. This review attempted to analyze a number of bacterial products as starting factors triggering this process. APSGN can be reproduced experimentally in rabbits by intravenous administration of a heat-killed Streptococcus pyogenes culture. In our experiments, strains of serotypes 1, 4, 12, 15, 22 were used. They produced M-proteins and had the ability to bind human and rabbit immunoglobulin G by interacting with the Fc part of the IgG molecule. In numerous series of experiments, evidence was obtained regarding the initiating role of GAS IgGFc-receptor proteins in developing APSGN. Recent studies confirmed the role of streptococcal IgGFc-binding proteins in the initiation of glomerulonephritis after animals were inoculated with temperature-killed IgGFc-positive GAS. This approach excluded a large group of bacterial extracellular agents from the list of APSGN-initiating candidates. An unconventional view on the pathogenesis of GAS-infection-coupled complications may allow approaching their prevention or new treatment strategies.

Острый постстрептококковый гломерулонефрит обычно возникает как осложнение после перенесенной стрептококковой инфекции в силу несвоевременной или неадекватной антибиотикотерапии. Этиология постстрептококкового гломерулонефрита изучена достаточно полно. И клиницисты, и микробиологи сегодня не отрицают главенствующую роль Streptococcus pyogenes (стрептококк серологической группы А, СГА). Обычно, возникновение гломерулонефрита принято связывать с так называемой «нефритогенностью» СГА, о чём нередко судят по появлению и накоплению в крови больных антител к антигенам и экстрацеллюлярным продуктам стрептококковой клетки. Данная трактовка достаточно вольная и скорее всего свидетельствует о принадлежности штамма, а не о его нефритогенности. Многим продуктам СГА разные авторы отводили и до сих пор приписывают роль ведущего «нефритогенного» фактора. На роль нефритогена претендуют перекрестно-реагирующие антигены, стрептокиназа, цистеиновая протеиназа, эндострептозин – белок клеточной мембраны СГА, фермент глицеральдегид-3-фосфат-дегидрогеназа обладающий тропностью к плазмину. Вопрос требует тщательного анализа, поскольку перечисленные стрептококковые продукты встречаются в почечных биоптатах, как и антитела к ним в крови больных. Что касается самого понятия «нефритогенность», то на сегодня оно убедительно не привязано ни к одному конкретному продукту стрептококковой клетки. На протяжении многих лет многие предполагаемые стрептококковые нефритогенные антигены изучались без определенного подтверждения их связи с гломерулонефритом. Рассмотрению последних посвящен данный обзор на примере генеза острого гломерулонефрита и анализа ряда бактериальных продуктов в качестве пусковых звеньев процесса. Процесс может быть воспроизведен экспериментально на кроликах путем внутривенного введения убитой нагреванием культуры Streptococcus pyogenes. В наших опытах использовались штаммы M-типов 1, 4, 12, 15, 22. Они продуцировали М-протеины и обладали способностью связывать иммуноглобулин G человека и кролика за счет взаимодействия с Fc-частью молекулы IgG. В многочисленных сериях экспериментов получен ряд доказательств, непосредственно указывающих на роль IgGFc-рецепторных белков СГА в качестве нефритогенного фактора, инициирующего острое воспаление клубочкового аппарата почек. Работы последних лет, несмотря на условность схем моделирования, подтвердили роль стрептококковых Fcγ-связывающих белков в инициации гломерулонефрита при введении животным убитых IgGFc-позитивных СГА. Такой подход исключал из числа кандидатов в инициирующие факторы большую группу бактериальных внеклеточных агентов. В данном обзоре мы постарались подробнее остановиться на начальной стадии острого постстрептококкового гломерулонефрита, на природе его пусковых звеньев, рассчитывая пробудить интерес к данной проблеме с целью изучения механизмов неиммунного связывания иммуноглобулинов патогенными микроорганизмами в постинфекционной патологии. Нестандартный взгляд на патогенез постинфекционных осложнений СГА-инфекции может позволить, в отличие от иных подходов, по-новому подойти к их профилактике или лечению, что подчеркнет перспективность приведенных представлений.

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