Reduction of host cell mitochondrial activity as Mycobacterium leprae's strategy to evade host innate immunity.

Reduction of host cell mitochondrial activity as Mycobacterium leprae's strategy to evade host innate immunity.
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DOI:
10.1111/imr.12962
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发表时间:
2021-05
影响因子:
8.7
通讯作者:
--
中科院分区:
医学1区
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--
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麻风病是由麻风分枝杆菌或麻风分枝杆菌病引起的一种令人非常恐惧的致残传染病,每年影响全世界约20万人。在宿主-病原体相互作用过程中,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,能量代谢对控制细胞内病原体和白细胞分化的影响已经变得更加明显。线粒体除了激活炎性体、异种吞噬和细胞凋亡外,还通过控制氧化还原代谢和能量流动,在调节新发现的免疫信号通路中发挥关键作用。同样,这种细胞器,其起源可能是一种阿尔法变形菌,直接控制试图入侵其生态位的细胞内病原体,这是一项以数十亿年共同进化为代价的壮举。在本综述中,我们讨论了宿主细胞线粒体活性降低在麻风分枝杆菌感染过程中的作用,以及麻风分枝杆菌和宿主先天免疫的相应命运。可以想象,抑制线粒体能量代谢是麻风分枝杆菌为逃避异种吞噬和宿主免疫反应而开发的一种被忽视的新机制。
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 feat 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.
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