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CYLD的上调增强了单核细胞增生李斯特菌诱导的THP-1细胞凋亡。

Up-regulation of CYLD enhances Listeria monocytogenes induced apoptosis in THP-1 cells.

作者信息

Xu Changzhi, Yang Ling, Yuan Yuan, Du Fei, Wang Shumin, Wang Xiangfang, Zhu Lin, Zhang Buchang, Weaver David

机构信息

Institute of Health Sciences, Anhui University, Hefei, Anhui 230601, PR China.

The Central Laboratory of Binhu Hospital, The Third Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, PR China.

出版信息

Microb Pathog. 2016 Jan;90:50-4. doi: 10.1016/j.micpath.2015.10.007. Epub 2015 Nov 3.

DOI:10.1016/j.micpath.2015.10.007
PMID:26545866
Abstract

Listeria monocytogenes (Lm), a facultative anaerobic gram-positive bacterium, causes listeriosis. Immune cell apoptosis is considered to be one pathogenic factor for listeriosis. As a deubiquitinase, CYLD is an important regulator both in innate immune response and apoptosis by negatively modulating NF-κB pathway. However the role of CYLD in Lm induced apoptosis remains unclear. Here we found that CYLD is significantly up-regulated in macrophages upon its infection. There is a moderate decrease in Lm proliferation and apoptotic cells in siRNA-induced CYLD knockdown THP-1 cells. Thereby CYLD may be involved in cell apoptosis mediated by Lm infection and its proliferation.

摘要

单核细胞增生李斯特菌(Lm)是一种兼性厌氧革兰氏阳性菌,可引起李斯特菌病。免疫细胞凋亡被认为是李斯特菌病的一个致病因素。作为一种去泛素化酶,CYLD通过负向调节NF-κB通路,在先天免疫反应和细胞凋亡中都是重要的调节因子。然而,CYLD在Lm诱导的细胞凋亡中的作用仍不清楚。在此我们发现,巨噬细胞在被Lm感染后CYLD显著上调。在siRNA诱导的CYLD敲低的THP-1细胞中,Lm增殖和凋亡细胞有适度减少。因此CYLD可能参与Lm感染介导的细胞凋亡及其增殖过程。

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