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EV71 infection induces cell apoptosis through ROS generation and SIRT1 activation
Author(s) -
Li Hongyan,
Bai Zhenzi,
Li Chenghua,
Sheng Chuanlun,
Zhao Xiaonan
Publication year - 2020
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29628
Subject(s) - apoptosis , reactive oxygen species , programmed cell death , inflammation , proinflammatory cytokine , microbiology and biotechnology , sirtuin 1 , downregulation and upregulation , tumor necrosis factor alpha , sirtuin , chemistry , biology , immunology , cancer research , biochemistry , acetylation , gene
Several studies have substantiated the correlation between reactive oxygen species (ROS) and Sirtuin 1 (SIRT1). Normally, enterovirus 71 (EV71) is associated with severe clinical manifestations and death. However, the effect of EV71 on the induction of cellular death and the interplay between ROS/SIRT1 in cell death has not been confirmed yet. In the current study, an increase in the number of apoptotic cells was observed as soon as the EV71 infection was initiated in cells and mice. Furthermore, EV71 infection also promoted a rise in the levels of three commonly known proinflammatory cytokines, interleukin 1β (IL‐1β), IL‐6, and tumor necrosis factor‐α. During EV71‐induced apoptosis in the different cell lines, ROS generation and SIRT1 downregulation were observed. Further investigations showed that the administration of ROS inhibitor, N‐acetyl‐ l ‐cysteine (NAC), reduced the level of apoptosis and inflammation, reduced EV71 propagation, and increased SIRT1 expression in EV71‐infected cells. In addition, combined administration of NAC and EX527 (SIRT1 inhibitor) restored apoptosis in the EV71‐infected cells, which was reduced due to NAC. This data demonstrated that ROS generation is positively associated with EV71‐induced apoptosis and inflammation, while this effect could be reversed by SIRT1 inhibition. Collectively, we have shown that EV71 induces apoptosis and inflammation by promoting ROS generation and reducing SIRT1 expression.