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Новый механизм резистентности к антибиотикам у бактерий

Serpent, 01.03.2014 20:20
картинка: Strep.pngУстойчивость (резистентность) микроорганизмов к антибиотикам, характерная для многих патогенных видов бактерий, представляет собой широко распространенный феномен и серьезнейшую проблему современной медицины. Достаточно вспомнить огромное число внутрибольничных инфекций, вызываемых высокоустойчивыми штаммами метициллин-резистентного Staphylococcus aureus (MRSA). Еще один пример – по данным ВОЗ, для 19% зарегистрированных в 2011 году случаев туберкулеза была отмечена множественная резистентность к антибиотикам.

Обычно бактерии приобретают резистентность в результате мутаций или же в результате горизонтального переноса генов резистентности от других видов бактерий. Эти постоянно идущие процессы провоцируют настоящую «гонку вооружений», вынуждая ученых постоянно искать и разрабатывать новые антибиотики. Соответственно, изучение механизмов резистентности представляется особенно важным.

В опубликованной в журнале Chemistry & Biology работе исследователи из Института Скриппса под руководством Ben Shen представили результаты изучения механизмов резистентности бактерий Streptomyces platensis к собственным антибиотикам. Относительно недавно из этого микроорганизма были выделены 2 новых антибиотика – платенсимицин (platensimycin, PTM) и платенцин (platencin, PTN). Оба вещества действуют, ингибируя процесс синтеза жирных кислот, необходимый в частности для формирования клеточной стенки бактерий. При этом платенсимицин непосредственно ингибирует один из ферментов синтеза (FabF), а платенцин – 2 фермента (FabF и FabH), активных на разных стадиях синтеза.

Авторы установили, что за устойчивость к антибиотикам у продуцирующих их штаммов Streptomyces platensis ответственны 2 механизма. Один из них обеспечивается модификацией мишени обоих антибиотиков – фермента FabF из локуса синтазы жирных кислот. В результате мутации данный фермент становится нечувствительным к действию антибиотика. Такой механизм обеспечения резистентности является «классическим» и известен довольно давно, однако в рассматриваемом случае он является второстепенным.

Основной же механизм реализуется за счет функциональной замены фермента, чувствительного к соответствующим антибиотикам, альтернативным нечувствительным ферментом. Последний кодируется генами ptmP3 и ptnP3 из биосинтетического кластера платенсимицина и платенцина соответственно. Примечательно, что ptmP3/ptnP3 кодируют 1 белок, функционально замещающий одновременно 2 фермента (FabF и FabH). Такой модифицированный механизм биосинтеза жирных кислот и соответствующий механизм устойчивости к антибиотикам описаны впервые. Соответственно, эти данные имеют большое значение для разработки будущих антибиотиков, нацеленных на бактериальный цикл синтеза жирных кислот.
авторский текст

Источник: Peterson RM, Huang T, Rudolf JD, Smanski MJ, Shen B. Mechanisms of Self-Resistance in the Platensimycin- and Platencin-Producing Streptomyces platensis MA7327 and MA7339 Strains. Chem Biol. 2014 Feb 18.

Подпись к рисунку: Снимок культуры Streptomyces sp. на предметном стекле. Изображение взято из Википедии.
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