In response to bacterial infection, epithelial cells undergo several types of cell death, including apoptosis, necrosis, pyroptosis, and necroptosis, which serve to expel the infected cells and activate the innate and acquired immune responses. Shigella initially invades macrophages and subsequently surrounding enterocytes; the pathogen executes macrophage cell death but prevents epithelial cell death in order to maintain its foothold for replication. To this end, Shigella delivers versatile effector proteins via the type III secretion system (T3SS), allowing it to efficiently colonize the intestinal epithelium. In this article, we review insights into the mechanisms underlying circumvention of the host cell death by Shigella, as an example of bacterial fine-tuning of host cell death pathways.

为响应细菌感染，上皮细胞经历多种类型的细胞死亡，包括细胞凋亡、坏死、细胞焦亡和坏死性凋亡，这有助于排出受感染的细胞并激活先天性和获得性免疫反应。志贺氏菌最初侵入巨噬细胞，随后侵入肠细胞；病原体执行巨噬细胞死亡，但阻止上皮细胞死亡，以维持其复制立足点。为此，志贺氏菌通过 III 型分泌系统 (T3SS) 提供多功能效应蛋白，使其能够有效地定植肠上皮。在本文中，我们回顾了对志贺氏菌绕过宿主细胞死亡的潜在机制的见解，作为细菌微调宿主细胞死亡途径的一个例子。