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传染性支气管炎病毒感染在鸡巨噬细胞HD11细胞复制过程中诱导细胞凋亡。

Infectious Bronchitis Virus Infection Induces Apoptosis during Replication in Chicken Macrophage HD11 Cells.

作者信息

Han Xiaoxiao, Tian Yiming, Guan Ru, Gao Wenqian, Yang Xin, Zhou Long, Wang Hongning

机构信息

Key Laboratory of Bio-Resources and Eco-Environment, Ministry of Education, College of Life Science, Sichuan University, Chengdu 610064, China.

Animal Disease Prevention and Food Safety Key Laboratory of Sichuan Province, Chengdu 610064, China.

出版信息

Viruses. 2017 Jul 26;9(8):198. doi: 10.3390/v9080198.

Abstract

Avian infectious bronchitis has caused huge economic losses in the poultry industry. Previous studies have reported that infectious bronchitis virus (IBV) infection can produce cytopathic effects (CPE) and apoptosis in some mammalian cells and primary cells. However, there is little research on IBV-induced immune cell apoptosis. In this study, chicken macrophage HD11 cells were established as a cellular model that is permissive to IBV infection. Then, IBV-induced apoptosis was observed through a cell viability assay, morphological changes, and flow cytometry. The activity of caspases, the inhibitory efficacy of caspase-inhibitors and the expression of apoptotic genes further suggested the activation of apoptosis through both intrinsic and extrinsic pathways in IBV-infected HD11 cells. Additionally, ammonium chloride (NH₄Cl) pretreated HD11 cells blocked IBV from entering cells and inhibited IBV-induced apoptosis. UV-inactivated IBV also lost the ability of apoptosis induction. IBV replication was increased by blocking caspase activation. This study presents a chicken macrophage cell line that will enable further analysis of IBV infection and offers novel insights into the mechanisms of IBV-induced apoptosis in immune cells.

摘要

禽传染性支气管炎给家禽业造成了巨大的经济损失。先前的研究报道,传染性支气管炎病毒(IBV)感染可在一些哺乳动物细胞和原代细胞中产生细胞病变效应(CPE)和凋亡。然而,关于IBV诱导免疫细胞凋亡的研究很少。在本研究中,建立了对IBV感染敏感的鸡巨噬细胞HD11细胞作为细胞模型。然后,通过细胞活力测定、形态变化和流式细胞术观察IBV诱导的凋亡。半胱天冬酶的活性、半胱天冬酶抑制剂的抑制效果以及凋亡基因的表达进一步表明,在IBV感染的HD11细胞中,凋亡通过内源性和外源性途径被激活。此外,氯化铵(NH₄Cl)预处理的HD11细胞可阻止IBV进入细胞并抑制IBV诱导的凋亡。紫外线灭活的IBV也失去了诱导凋亡的能力。通过阻断半胱天冬酶激活可增加IBV复制。本研究提供了一种鸡巨噬细胞系,这将有助于进一步分析IBV感染,并为IBV诱导免疫细胞凋亡的机制提供新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4890/5580455/39710796ffd9/viruses-09-00198-g001.jpg

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