Ozone exposure in the culture medium inhibits enterovirus 71 virus replication and modulates cytokine production in rhabdomyosarcoma cells
Ozone exposure in the culture medium inhibits enterovirus 71 virus replication and modulates cytokine production in rhabdomyosarcoma cells
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DOI：
10.1016/j.antiviral.2007.07.004
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发表时间：
2007-12-01
影响因子：
7.6
通讯作者：
Cheng, Yi-Chen
中科院分区：
文献类型：
--
作者：
Lin, Ya-Ching;Juan, Hao-Chan;Cheng, Yi-Chen
在本研究中，臭氧暴露对肠道病毒71型（EV 71）复制和相关细胞因子产生的影响进行了研究。将横纹肌肉瘤细胞（RD）分别暴露于0.5、1、1.5和2 ppm的臭氧或过滤空气中，在感染前或感染后1或2 h。结果表明，在适当的臭氧浓度下，1.5或2 ppm时，臭氧暴露限制了病毒产生，延长了细胞存活时间，并调节了与EV 71感染相关的细胞因子产生。当未感染的细胞暴露于1.5或2 ppm的臭氧1小时后，IL-1 β，IL-6和TNF-α的产生。在感染后48 h内，对EV 71复制产生抑制作用。虽然感染的细胞暴露于1.5或2 ppm的臭氧2小时，臭氧不影响RD细胞响应EV 71感染的细胞因子产生。结果表明，臭氧对细胞因子的诱导作用仅见于未感染细胞。臭氧诱导的细胞因子在EV 71感染开始前产生抗病毒作用，这被证明有利于抑制随后的EV 71感染。(C)2007 Elsevier B. V.保留所有权利。
In the present study, the effects of ozone exposure on enterovirus 71 (EV71) replication and related cytokine production were investigated. Rhabdomyosarcoma cells (RD) were exposed to 0.5, 1, 1.5 and 2ppm ozone or filtered air under different exposure regimens before or after infection for 1 or 2 h. The results revealed that at a proper concentration of ozone, e.g., 1.5 or 2 ppm, ozone exposure restricted virus production, prolonged survival time of cells and modulated cytokine production related to EV71 infection. Upon exposure of non-infected cells to ozone at 1.5 or 2 ppm for 1 h, the production of IL-1 beta, IL-6 and TNF-alpha. was primed and boosted by the subsequent EV71 infection, generating an inhibitory effect on EV71 replication during the post-infection period of 48 h. While infected cells were exposed to ozone for 2 h at 1.5 or 2 ppm, ozone did not affect cytokine production by RD cells in response to EV71 infection. The data showed that ozone effect on induction of cytokine was only found in uninfected cells. The ozone-induced cytokines produced prior to the onset of EV71 infection generated antiviral effects, which proved beneficial in suppressing the subsequent EV71 infection. (C) 2007 Elsevier B.V. All rights reserved.