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Журнал микробиологии, эпидемиологии и иммунобиологии. 2017; : 78-90

ПСЕВДОТУБЕРКУЛЕЗ: ПАТОГЕНЕТИЧЕСКОЕ ЗНАЧЕНИЕ КЛЕТОК ВРОЖДЕННОГО ИММУНИТЕТА

Сомова Л. М., Плехова Н. Г., Дробот Е. И., Ляпун И. Н.

https://doi.org/10.36233/0372-9311-2017-5-78-90

Аннотация

В обзоре обобщены новые данные о механизмах врожденной иммунной защиты при инфекциях, вызываемых патогенными Yersiniae, что в значительной степени было обусловлено комплексными разработками относительно уникальной пары генетически родственных возбудителей Y. pseudotuberculosis/Y. pestis. Проведенные нами ранее исследования выявили морфологический субстрат относительного гранулоцитарного иммунодефицита, обусловливающего характерные патоморфологические особенности псевдотуберкулеза. К настоящему времени получен ы доказательства того, что патогенные для человека виды Yersinia преимущественно инактивируют защитную функцию клеток врожденного иммунитета, что является важной стратегией, с помощью которой эти бактерии избегают элиминации и вызывают заболевание. В ответ на заражение патогенными Yersiniae фундаментальную роль в первичной иммунной защите и в ограничении первоначального распространения бактерий в организме играют нейтрофилы (ПЯЛ ), которые используют несколько механизмов для ликвидации бактерий, таких как фагоцитоз, оксидативный стресс, секреторная дегрануляция, образование нейтрофильных внеклеточных ловушек, эффероцитоз. Инфицированные ПЯЛ могут действовать как промежуточный хозяин для последующей невоспалительной инфекции макрофагов. Дальнейшее раскрытие вопросов, касающихся первичной антиинфекционной защиты при Yersinia инфекциях даст ключ к пониманию иммунопатогенеза эпидемического псевдотуберкулеза (дальневосточной скарлатиноподобной лихорадки) и в целом иерсиниозов.
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Journal of microbiology, epidemiology and immunobiology. 2017; : 78-90

PSEUDOTUBERCULOSIS: PATHOGENETIC VALUE OF INNATE IMMUNITY CELLS

Somova L. M., Plekhova N. G., Drobot E. I., Lyapun I. N.

https://doi.org/10.36233/0372-9311-2017-5-78-90

Abstract

Novel data on mechanisms of innate immunity during infections with pathogenic Yersiniae are summarized in the review, that was mostly determined by complex developments regarding a unique pair of genetically related causative agents Y. pseudotuberculosis/Y. pestis. Our previous studies have revealed a morphological substrate of relative granulocyte immune deficiency that determines characteristic pathomorphologic features of pseudotuberculosis. To date, evidence has been obtained, that pathogenic for human Yersinia predominately activate protective function of innate immunity cells that is an important strategy to avoid elimination and cause the disease for the bacteria. Neutrophils (PMNs) play a fundamental role in response to infection by pathogenic Yersiniae in primary immune response and limit of primary spread of bacteria that use several mechanisms of eradication ofbacteria, e.g.: phagocytosis, oxidative stress, secretory degranulation, formation of neutrophil extracellular traps, efferocytosis. Infected PMNs can act as an intermediate host for consequent non-inflammatory infection of macrophages. Further elaboration of questions relating to primary anti-infection protection during Yersinia infections gives a key to understanding of immune pathogenesis of epidemic pseudotuberculosis (far Eastern scarlet-like fever) and yersiniosis in general.
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50. Westermark L., Fahgren A., Fallman M. Yersinia pseudotuberculosis efficiently escapes polymorphonuclear neutrophils during early infection. Infect. Immun. 2014, 82 (3): 1181-1191.