Leprosy is a much-feared incapacitating infectious disease caused by Mycobacterium leprae or M lepromatosis, annually affecting roughly 200,000 people worldwide. During host-pathogen interaction, M leprae subverts the immune response, leading to development of disease. Throughout the last few decades, the impact of energy metabolism on the control of intracellular pathogens and leukocytic differentiation has become more evident. Mitochondria play a key role in regulating newly-discovered immune signaling pathways by controlling redox metabolism and the flow of energy besides activating inflammasome, xenophagy, and apoptosis. Likewise, this organelle, whose origin is probably an alphaproteobacterium, directly controls the intracellular pathogens attempting to invade its niche, a feature conquered at the expense of billions of years of coevolution. In the present review, we discuss the role of reduced host cell mitochondrial activity during M leprae infection and the consequential fates of M leprae and host innate immunity. Conceivably, inhibition of mitochondrial energy metabolism emerges as an overlooked and novel mechanism developed by M leprae to evade xenophagy and the host immune response.

中文翻译：

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降低宿主细胞线粒体活性作为麻风分枝杆菌逃避宿主先天免疫的策略

麻风病是一种令人恐惧的致残传染病，由麻风分枝杆菌或麻风分枝杆菌引起，每年影响全球约 200,000 人。在宿主-病原体相互作用期间，麻风分枝杆菌破坏免疫反应，导致疾病的发展。在过去的几十年里，能量代谢对细胞内病原体控制和白细胞分化的影响变得更加明显。线粒体通过控制氧化还原代谢和能量流动以及激活炎性体、异体自噬和细胞凋亡，在调节新发现的免疫信号通路中发挥关键作用。同样，这种起源可能是α变形杆菌的细胞器直接控制着试图侵入其生态位的细胞内病原体，这一特征是以数十亿年的协同进化为代价被征服的。在本综述中，我们讨论了麻风分枝杆菌感染期间宿主细胞线粒体活性降低的作用以及麻风分枝杆菌的后续命运和宿主先天免疫。可以想象，抑制线粒体能量代谢是麻风分枝杆菌为逃避异体自噬和宿主免疫反应而开发的一种被忽视的新机制。