Chen Kaiwen W, Brodsky Igor E
Immunology Translational Research Programme, Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore; Immunology Programme, Life Sciences Institute, National University of Singapore, Singapore, Singapore.
Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, United States; Department of Microbiology, University of Pennsylvania Perelman School of Medicine, United States.
Curr Opin Microbiol. 2023 Feb;71:102256. doi: 10.1016/j.mib.2022.102256. Epub 2022 Dec 28.
Cell death in response to infection is conserved across all kingdoms of life. In metazoans, cell death upon bacterial infection is primarily carried out by the cysteine and aspartate protease and receptor-interacting serine/threonine protein kinase families. The Gram-negative bacterial genus Yersinia includes pathogens that cause disease in humans and other animals ranging from plague to gastrointestinal infections. Pathogenic Yersiniae express a type-III secretion system (T3SS), which translocates effectors that disrupt phagocytosis and innate immune signaling to evade immune defenses and replicate extracellularly in infected tissues. Blockade of innate immune signaling, disruption of the actin cytoskeleton, and the membrane-disrupting activity of the T3SS translocon pore, are all sensed by innate immune cells. Here, we discuss recent advances in understanding the pathways that regulate Yersinia-induced cell death, and how manipulation of these cell death pathways over the course of infection promotes bacterial dissemination or host defense.
响应感染的细胞死亡在所有生命王国中都是保守的。在多细胞动物中，细菌感染后的细胞死亡主要由半胱氨酸和天冬氨酸蛋白酶以及受体相互作用的丝氨酸/苏氨酸蛋白激酶家族来执行。革兰氏阴性细菌耶尔森氏菌属包括在人类和其他动物中引起疾病的病原体，范围从鼠疫到胃肠道感染。致病性耶尔森氏菌表达III型分泌系统（T3SS），该系统转运效应蛋白，这些效应蛋白破坏吞噬作用和先天免疫信号传导，以逃避免疫防御并在感染组织中进行细胞外复制。先天免疫信号的阻断、肌动蛋白细胞骨架的破坏以及T3SS转位子孔的膜破坏活性，都被先天免疫细胞感知到。在这里，我们讨论了在理解调节耶尔森氏菌诱导的细胞死亡的途径方面的最新进展，以及在感染过程中对这些细胞死亡途径的操纵如何促进细菌传播或宿主防御。
