Cytokines and inflammationCytokines and inflammationЦитокины и воспаление1684-7849Eco-Vector63014810.17816/CI630148ReviewsНаучные обзорыReview ArticleRole of inflammation in the pathogenesis of novel coronavirus infectionРоль воспаления в патогенезе новой коронавирусной инфекцииhttps://orcid.org/0000-0002-5243-8085HJA-1825-20226093-7430KlimovNikolay A.КлимовНиколай Анатольевич
Russian Federation

MD, Cand. Sci. (Medicine)

канд. мед. наук

nklimov@mail.ruhttps://orcid.org/0000-0002-8228-42407003758888K-2087-20132064-7584SimbirtsevAndrey S.СимбирцевАндрей Семенович
Russian Federation

MD, Dr. Sci. (Medicine), Professor, Corresponding Member of the Russian Academy of Sciences

д-р мед. наук, профессор, член-корреспондент РАН

simbas@mail.ruInstitute of Experimental MedicineИнститут экспериментальной медициныState Research Institute of Highly Pure BiopreparationsГосударственный научно-исследовательский институт особо чистых биопрепаратов170820242512202320416280904202405082024Copyright ©; 2023, Eco-VectorCopyright ©; 2023, Эко-Вектор2023Eco-VectorЭко-Векторhttps://creativecommons.org/licenses/by-nc-nd/4.0/https://cijournal.ru/1684-7849/article/view/630148

The activation of various types of epithelial, endothelial, and immunocompetent cells, along with hyperproduction of cytokines and other proinflammatory mediators and activation of the complement system, plays a crucial in the pathogenesis of coronavirus disease 2019 (COVID-19). These conditions leads to severe inflammation and acute respiratory distress syndrome. Hyperinflammatory reactions in the lungs and other tissues result in significant tissue damage and organ dysfunction. A specific feature of severe acute respiratory syndrome coronavirus 2 infection is the combination of cell death and inflammation. In COVID-19, not only pneumocytes but also many other cells are killed. These cells undergo programed cell death through three main pathways: apoptosis, pyroptosis, and necroptosis. These processes help protect organisms from intracellular pathogens by releasing them from infected cells, which then bind to specific receptors and antibodies, undergo opsonization, and are phagocytosed. Localized inflammation aims to eliminate these pathogens, but severe inflammation is an important component of the immunopathogenesis of COVID-19. The immunopathogenesis of COVID-19, particularly the role of inflammation in the development of severe clinical signs, is now largely understood. This disease has a complex immunopathology, including excessive activation of adaptive and innate branches of the immune system and interactions between immune cells and affected tissues.

В патогенезе COVID-19 важную роль играет активация различных типов клеток эпителия, эндотелия и иммунокомпетентных клеток, что сопровождается гиперпродукцией цитокинов и других провоспалительных медиаторов, активацией системы комплемента и служит причиной неадекватно сильного воспаления с развитием острого респираторного дистресс-синдрома. Развивающаяся в тканях лёгких и в других тканях гипервоспалительная реакция приводит к значительным тканевым изменениям и нарушениям функционирования органов. Особенностью инфекции, вызываемой вирусом SARS-CoV-2, является сочетание гибели клеток с воспалением. При COVID-19 происходит гибель не только пневмоцитов, но и многих других клеток. Механизмом разрушения клеток выступает программированная клеточная гибель, которая осуществляется через главные, тесно связанные между собой пути: апоптоз, пироптоз и некроптоз. Эти процессы способствуют защите организма от внутриклеточных патогенов: инфицированные клетки гибнут, освобождаемые из них патогены, в том числе незрелые, подвергаются связыванию специфическими рецепторами, антителами, опсонизации и фагоцитозу. Формируется локальное воспаление, предназначенное для элиминации патогена. Однако индукция слишком высокого уровня воспаления является важной составляющей иммунопатогенеза COVID-19. В настоящее время иммунопатогенез COVID-19, в частности роль воспаления в развитии тяжёлых клинических проявлений инфекции, во многом изучен. Стало очевидным, что при данном заболевании наблюдается сложная иммунопатология, включающая чрезмерную активацию адаптивной и врождённой ветвей иммунной системы, а также взаимодействие между различными иммунными клетками и поражёнными тканями.

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