Нейтрофилы: неоднозначная роль в патогенезе туберкулеза

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Туберкулез (ТБ) до сих пор является важной нерешенной медицинской проблемой. Примерно четверть человечества заражена Mycobacterium tuberculosis, и у 5–10% рано или поздно развивается ТБ. Макрофаги и Т-лимфоциты CD4+ являются основными иммунными клетками, противостоящими ТБ-инфекции. Гораздо меньше известно о роли нейтрофилов при ТБ. Нейтрофилы, короткоживущие лейкоциты, в числе первых реагируют на проникновение инфекции, мигрируют в очаг воспаления и поглощают микобактерии в легких. С одной стороны, есть свидетельства защитной роли нейтрофилов за счет продукции пептидов, подавляющих рост микобактерий, усиления активации Т-лимфоцитов CD4+ и миграции дендритных клеток в лимфоузлы. С другой стороны, инфицирование генетически чувствительных к ТБ животных приводит к избыточному притоку нейтрофилов в легкие, формированию некротических гранулем и быстрой гибели. Нейтрофилы напрямую или опосредованно воздействуют на микобактерии, используя различные окислительные и неокислительные реакции, а также образуя нейтрофильные внеклеточные ловушки (NETs). Фагоцитоз микобактерий нейтрофилами стимулирует выделение ими множества провоспалительных медиаторов, поэтому нейтрофилы являются активными участниками воспаления на всех стадиях развития инфекционного процесса. В конечном итоге нейтрофилы погибают путем апоптоза или некроза. Гибель нейтрофилов путем некроза, инициируемого активными формами кислорода, в свою очередь также провоцирует излишнее воспаление. В связи с этим велика вероятность того, что именно нейтрофилы способствуют переходу ТБ в терминальную стадию, участвуя в распаде легочной ткани. Кроме того, несмотря на то что эволюционно нейтрофилы имеют достаточно возможностей воздействия на патоген, по-видимому, сами по себе они не обладают достаточной бактерицидной активностью в отношении микобактерий вследствие формирования у последних механизмов защиты, позволяющих выживать внутри клеток. Таким образом, нейтрофилы фагоцитируют, но не убивают микобактерии и могут выступать в роли «троянского коня», экранируя бактерии от более эффективных защитных действий макрофагов. В этом обзоре мы обобщаем данные последних лет об участии нейтрофилов в туберкулезном воспалении. Мы обсуждаем неоднозначность их роли в патогенезе в зависимости от вирулентости микобактерий и генетических особенностей хозяина, динамику притока нейтрофилов в очаг воспаления и персистирование в начальной и хронической стадиях инфекции.

Об авторах

И. А. Линге

ФГБНУ Центральный НИИ туберкулеза

Автор, ответственный за переписку.
Email: iralinge@gmail.com
ORCID iD: 0000-0003-1535-5800

Линге Ирина Андреевна,  к.б.н., старший научный сотрудник лаборатории иммуногенетики отдела иммунологии 

107564, Москва, Яузская аллея, 2,

Тел.: 8 499 785-90-72

Россия

А. С. Апт

ФГБНУ Центральный НИИ туберкулеза

Email: alexapt0151@gmail.com
ORCID iD: 0000-0002-3683-3085

д.б.н., профессор, зав. лабораторией иммуногенетики отдела иммунологии 

Москва

Россия

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