The facultative intracellular pathogen Brucella abortus interacts with several organelles of the host cell to reach its replicative niche inside the endoplasmic reticulum. However, little is known about the interplay between the intracellular bacteria and the host cell mitochondria. Here, we showed that B. abortus triggers substantive mitochondrial network fragmentation, accompanied by mitophagy and the formation of mitochondrial Brucella-containing vacuoles during the late steps of cellular infection. Brucella-induced expression of the mitophagy receptor BNIP3L is essential for these events and relies on the iron-dependent stabilisation of the hypoxia-inducible factor 1α. Functionally, BNIP3L-mediated mitophagy appears to be advantageous for bacterial exit from the host cell as BNIP3L depletion drastically reduces the number of reinfection events. Altogether, these findings highlight the intricate link between Brucella trafficking and the mitochondria during host cell infection.

中文翻译：

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流产布鲁氏菌的宿主细胞出口需要 BNIP3L 介导的线粒体自噬


兼性细胞内病原体流产布鲁氏菌与宿主细胞的多个细胞器相互作用，以到达内质网内的复制生态位。然而，人们对细胞内细菌与宿主细胞线粒体之间的相互作用知之甚少。在这里，我们发现流产布鲁氏菌在细胞感染的后期阶段会引发实质性的线粒体网络断裂，并伴有线粒体自噬和含有布鲁氏菌的线粒体空泡的形成。布鲁氏菌诱导的线粒体自噬受体 BNIP3L 的表达对于这些事件至关重要，并且依赖于缺氧诱导因子 1α 的铁依赖性稳定。从功能上讲，BNIP3L 介导的线粒体自噬似乎有利于细菌从宿主细胞中退出，因为 BNIP3L 的消耗大大减少了再感染事件的数量。总而言之，这些发现强调了宿主细胞感染过程中布鲁氏菌运输与线粒体之间的复杂联系。