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NLRP3 炎性小体对 DF-1 细胞中传染性法氏囊病病毒复制的保护作用。

Protective effects of the NLRP3 inflammasome against infectious bursal disease virus replication in DF-1 cells.

机构信息

State Key Laboratory of Animal Nutrition, College of Animal Science and Technology, China Agricultural University, Beijing, 100193, China.

China Animal Husbandry Industry Co. Ltd, Beijing, 100070, China.

出版信息

Arch Virol. 2021 Jul;166(7):1943-1950. doi: 10.1007/s00705-021-05099-7. Epub 2021 May 12.

Abstract

Inflammatory responses are an important part of the innate immune response during viral infection. Various inflammasome complexes have been identified. The pyrin domain-containing 3 (NLRP3) inflammasome plays a critical role in detecting some RNA viruses, such as influenza virus. However, the effect of the NLRP3 inflammasome on infectious bursal disease virus (IBDV) replication is still unclear. Here, we report that IBDV-infection induces the transcription of NLRP3 inflammasome and IL-1β genes in the immortalized chicken embryo fibroblast cell line DF-1. Inhibition of caspase-1 by Belnacasan (VX-765) suppressed the transcription of IL-1β, reduced cell lysis, and significantly promoted IBDV replication in DF-1 cells. Furthermore, knockdown of NLRP3 by small interfering RNA promoted IBDV replication in the host cells. Thus, IBDV can induce NLRP3 inflammasome activation in DF-1 cells through a mechanism requiring viral replication, revealing a new antiviral mechanism employed by the host.

摘要

炎症反应是病毒感染期间固有免疫反应的重要组成部分。已经鉴定出各种炎性体复合物。含pyrin 结构域的 3(NLRP3)炎性体在检测某些 RNA 病毒(如流感病毒)方面起着关键作用。然而,NLRP3 炎性体对传染性法氏囊病病毒(IBDV)复制的影响尚不清楚。在这里,我们报告 IBDV 感染诱导永生化鸡胚成纤维细胞系 DF-1 中 NLRP3 炎性体和 IL-1β 基因的转录。Belnacasan(VX-765)抑制半胱天冬酶-1 的活性抑制了 IL-1β 的转录,减少了细胞裂解,并显著促进了 DF-1 细胞中的 IBDV 复制。此外,通过小干扰 RNA 敲低 NLRP3 促进了宿主细胞中的 IBDV 复制。因此,IBDV 可以通过需要病毒复制的机制诱导 DF-1 细胞中 NLRP3 炎性体的激活,揭示了宿主采用的一种新的抗病毒机制。

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