In addition to housing the major energy-producing pathways in cells, mitochondria are active players in innate immune responses. One critical way mitochondria fulfill this role is by releasing damage-associated molecular patterns (mtDAMPs) that are recognized by innate sensors to activate pathways including, but not limited to, cytokine expression, selective autophagy, and cell death. Mitochondrial reactive oxygen species (mtROS) is a multifunctional mtDAMP linked to pro- and antimicrobial immune outcomes. Formed as a by-product of energy generation, mtROS links mitochondrial metabolism with downstream innate immune responses. As a result, altered cellular metabolism can change mtROS levels and impact downstream antimicrobial responses in a variety of ways. MtROS has emerged as a particularly important mediator of pathogenesis during infection with Mycobacterium tuberculosis (Mtb), an intracellular bacterial pathogen that continues to pose a significant threat to global public health. Here, we will summarize how Mtb modulates mtROS levels in infected macrophages and how mtROS dictates Mtb infection outcomes by controlling inflammation, lipid peroxidation, and cell death. We propose that mtROS may serve as a biomarker to predict tuberculosis patient outcomes and/or a target for host-directed therapeutics.

除了容纳细胞中主要的能量产生途径外，线粒体还是先天免疫反应的积极参与者。线粒体发挥这一作用的一个关键方式是释放损伤相关分子模式（mtDAMP），这些模式被先天传感器识别以激活途径，包括但不限于细胞因子表达、选择性自噬和细胞死亡。线粒体活性氧(mtROS) 是一种多功能 mtDAMP，与促免疫和抗菌免疫结果相关。mtROS 是能量产生的副产品，将线粒体代谢与下游先天免疫反应联系起来。因此，细胞代谢的改变可以改变 mtROS 水平并以多种方式影响下游抗菌反应。MtROS 已成为结核分枝杆菌(Mtb) 感染过程中特别重要的发病机制介质，结核分枝杆菌是一种细胞内细菌病原体，持续对全球公共卫生构成重大威胁。在这里，我们将总结 Mtb 如何调节受感染巨噬细胞中的 mtROS 水平，以及 mtROS 如何通过控制炎症、脂质过氧化和细胞死亡来决定 Mtb 感染结果。我们建议 mtROS 可以作为预测结核病患者预后的生物标志物和/或宿主导向治疗的靶点。