Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections
Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections
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DOI：
10.1002/jmv.20556
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发表时间：
2006-04-01
影响因子：
12.7
通讯作者：
Fujii, N
中科院分区：
文献类型：
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作者：
Okabayashi, T;Kariwa, H;Fujii, N
严重急性呼吸综合征（SARS）的发病机制尚不清楚，细胞因子失调被认为是有待探索的一种相关机制。我们比较了 SARS 冠状病毒 (SARS-CoV) 与其他呼吸道病毒（包括呼吸道合胞病毒 (RSV)、甲型流感病毒 (FluAV) 和人类副流感病毒 2 型 (hPIV2)）感染后 Caco2 细胞中的细胞因子谱。干扰素 (IFN) 系统（产生和反应）并未受到 SARS-CoV 感染的抑制。因此，IFN 预处理可抑制 SARS-CoV 复制。与 FluAV 和 hPIV2 相比，SARS-CoV 和 RSV 诱导高水平的 IL-6 和 RANTES。尽管 IL-6 大量产生，但 SARS-CoV 诱导的细胞因子信号传导抑制因子 3 (SOCS3) 的诱导水平显着低于 RSV。与炎症反应的诱导相关的 Toll 样受体 4 和 9 因 SARS-CoV 感染而上调。总的来说，炎症细胞因子的过度诱导和细胞因子信号传导的失调可能导致与 SARS 中“严重”炎症相关的免疫病理学。
The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS-CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS-CoV infection. Therefore, SARS-CoV replication was suppressed by pretreatment with IFN. SARS-CoV and RSV induced high levels of IL-6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling-3 (SOCS3) by SARS-CoV was significantly lower than that by RSV in spite of the significant production of IL-6. Toll-like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS-CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with "severe" inflammation in SARS.