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首页> 外文期刊>Infection and immunity >The interleukin 1beta-converting enzyme, caspase 1, is activated during Shigella flexneri-induced apoptosis in human monocyte-derived macrophages.
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The interleukin 1beta-converting enzyme, caspase 1, is activated during Shigella flexneri-induced apoptosis in human monocyte-derived macrophages.

机译：在人单核细胞衍生的巨噬细胞中，志贺氏菌诱导的凋亡过程中，白介素1β转换酶caspase 1被激活。

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摘要

Shigella, the etiological agent of bacillary dysentery, rapidly kills human monocyte-derived macrophages in vitro. Wild-type Shigella flexneri, but not a nonvirulent derivative, induced human macrophage apoptosis as determined by morphology and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL). Shigella-mediated macrophage cell death was blocked by the peptide inhibitors of caspases, acetyl-Tyr-Val-Ala-Asp-aldehyde (acetyl-YVAD-CHO) and acetyl-Tyr-Val-Ala-Asp-chloromethylketone (acetyl-YVAD-CMK). Protection from apoptosis by YVAD was observed in monocytes matured in the presence or absence of colony-stimulating factors (CSF) like macrophage-CSF or granulocyte-macrophage-CSF. Furthermore, lipopolysaccharide (LPS) or gamma interferon (IFN-gamma) rendered human macrophages partially resistant to Shigella cytotoxicity. Macrophages stimulated with either LPS or IFN-gamma were also protected by YVAD from Shigella-induced cell death. During Shigella infections of human macrophages, interleukin-1beta (IL-1beta) was cleaved to the mature form. IL-1beta maturation was severely retarded by YVAD, indicating that IL-1beta-converting enzyme (ICE; caspase 1) is activated in Shigella-induced apoptosis. The finding that Shigella induces apoptosis in human macrophages by activating ICE supports the hypothesis that the acute inflammation characteristic of shigellosis is initially triggered by apoptotic macrophages which release mature IL-1beta during programmed cell death.
机译：细菌性痢疾的病原菌志贺氏菌（Shigella）可在体外迅速杀死人单核细胞衍生的巨噬细胞。如形态和末端脱氧核苷酸转移酶介导的dUTP-生物素缺口末端标记（TUNEL）所确定的，野生型弗氏志贺氏菌而非非毒性衍生物诱导人巨噬细胞凋亡。志贺菌介导的巨噬细胞死亡被胱天蛋白酶，乙酰基-Tyr-Val-Ala-Asp-醛（乙酰基-YVAD-CHO）和乙酰基-Tyr-Val-Ala-Asp-氯甲基酮（乙酰基-YVAD- CMK）。在存在或不存在诸如巨噬细胞-CSF或粒细胞-巨噬细胞-CSF的集落刺激因子（CSF）的条件下成熟的单核细胞中，观察到了通过YVAD防止凋亡的保护作用。此外，脂多糖（LPS）或γ干扰素（IFN-γ）使人巨噬细胞部分抗志贺氏菌的细胞毒性。用LPS或IFN-γ刺激的巨噬细胞也被YVAD保护免受志贺氏菌诱导的细胞死亡。在人类巨噬细胞志贺氏菌感染期间，白介素-1β（IL-1beta）裂解为成熟形式。 IL-1beta成熟受到YVAD的严重阻碍，表明IL-1beta转换酶（ICE; caspase 1）在志贺氏菌诱导的细胞凋亡中被激活。志贺氏菌通过激活ICE诱导人类巨噬细胞凋亡的发现支持以下假说：志贺菌病的急性炎症特征最初是由程序性细胞死亡过程中释放成熟IL-1β的凋亡巨噬细胞触发的。

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