Mycobacterium tuberculosis (Mtb) is an etiologic pathogen of human tuberculosis (TB), a serious infectious disease with high morbidity and mortality. In addition, the threat of drug resistance in anti-TB therapy is of global concern. Despite this, it remains urgent to research for understanding the molecular nature of dynamic interactions between host and pathogens during TB infection. While Mtb evasion from phagolysosomal acidification is a well-known virulence mechanism, the molecular events to promote intracellular parasitism remains elusive. To combat intracellular Mtb infection, several defensive processes, including autophagy and apoptosis, are activated. In addition, Mtb-ingested phagocytes trigger inflammation, and undergo necrotic cell death, potentially harmful responses in case of uncontrolled pathological condition. In this review, we focus on Mtb evasion from phagosomal acidification, and Mtb interaction with host autophagy, apoptosis, and necrosis. Elucidation of the molecular dialogue will shed light on Mtb pathogenesis, host defense, and development of new paradigms of therapeutics.

中文翻译：

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分枝杆菌感染期间自噬、细胞凋亡和坏死中的宿主-病原体对话

结核分枝杆菌 (Mtb) 是人类结核病 (TB) 的病原体，是一种具有高发病率和死亡率的严重传染病。此外，抗结核治疗中耐药性的威胁是全球关注的问题。尽管如此，仍然迫切需要研究以了解结核病感染期间宿主和病原体之间动态相互作用的分子性质。虽然 Mtb 逃避吞噬溶酶体酸化是众所周知的毒力机制，但促进细胞内寄生的分子事件仍然难以捉摸。为了对抗细胞内 Mtb 感染，激活了几个防御过程，包括自噬和细胞凋亡。此外，Mtb 摄入的吞噬细胞会引发炎症，并发生坏死细胞死亡，在不受控制的病理状况下可能产生有害反应。在这次审查中，我们专注于 Mtb 逃避吞噬体酸化，以及 Mtb 与宿主自噬、细胞凋亡和坏死的相互作用。分子对话的阐明将阐明 Mtb 的发病机制、宿主防御和新疗法的发展。