畜牧兽医学报 ›› 2022, Vol. 53 ›› Issue (8): 2633-2641.doi: 10.11843/j.issn.0366-6964.2022.08.021

• 预防兽医 • 上一篇    下一篇

金黄色葡萄球菌对BV2细胞IFN-α生成的影响

卢婉青1, 赵莎莎1, 蒋松宏1, 童智子1, 黄丹妮1, 郭建华1,2, 吴俊伟1, 周洋1,2*   

  1. 1. 西南大学动物医学院, 重庆 402460;
    2. 西南大学医学研究院免疫学研究中心, 重庆 402460
  • 收稿日期:2021-12-20 出版日期:2022-08-23 发布日期:2022-08-23
  • 通讯作者: 周洋,主要从事免疫学研究,E-mail:anonymous17@163.com
  • 作者简介:卢婉青(2001-),女,安徽六安人,学士,主要从事宿主-病原相互作用研究,E-mail:2829064541@qq.com
  • 基金资助:
    国家自然科学基金资助项目(31802158)

Effect of Staphylococcus aureus on IFN-α Production in BV2 Cells

LU Wanqing1, ZHAO Shasha1, JIANG Songhong1, TONG Zhizi1, HUANG Danni1, GUO Jianhua1,2, WU Junwei1, ZHOU Yang1,2*   

  1. 1. College of Veterinary Medicine, Southwest University, Chongqing 402460, China;
    2. Immunology Research Center, Medical Research Institute, Southwest University, Chongqing 402460, China
  • Received:2021-12-20 Online:2022-08-23 Published:2022-08-23

摘要: 旨在探究金黄色葡萄球菌(Staphylococcus aureus,简称金葡菌)对小胶质细胞α干扰素(interferon α,IFN-α)生成的影响,本研究先用金葡菌感染BV2细胞,检测IFN-α的mRNA表达、分泌到细胞培养液上清的量以及TBK1/IRF3通路的激活情况,再分别用TBK1抑制剂BX-795和amlexanox、NF-κB抑制剂IMD-0354处理细胞,检测TBK1/IRF3的激活以及IFN-α水平。结果表明,BV2感染金葡菌后,IFN-α转录水平在3~12 h升高,6~12 h释放量增加,呈剂量依赖性,TBK1和IRF3的转录水平和蛋白水平未发生变化,但在1~12 h其磷酸化水平升高,表明金葡菌激活BV2细胞TBK1/IRF3通路,BX-795、amlexanox和IMD-0354处理细胞后,IRF3磷酸化水平降低,IFN-α生成减少,表明TBK1和NF-κB参与金葡菌促进BV2细胞生成IFN-α。综上所述,金葡菌感染BV2后促进IFN-α生成,且该过程依赖于TBK1和NF-κB,本结果为临床防治中枢神经系统感染金葡菌提供了可能靶点和理论基础。

关键词: 金黄色葡萄球菌, BV2, IFN-α, TBK1, IRF3

Abstract: To explore the influence of Staphylococcus aureus on IFN-α production and IFN-α mRNA expression in microglia cells. IFN-α released into the culture medium and TBK1/IRF3 signaling of BV2 cells were detected after BV2 cells were infected with S. aureus. TBK1/IRF3 pathway activation and IFN-α levels were detected after S. aureus infected BV2 cells which were treated by BX-795, amlexanox, IMD-0354 inhibitors, respectively. The results showed that IFN-α transcriptional levels increased from 3 to 12 hours post infection, and IFN-α release was enhanced from 6 to 12 hours post infection in a dose-dependent manner. TBK1 and IRF3 were not affected at both the mRNA and protein levels, but their phosphorylation was triggered from 1 to 12 hours, indicating that S. aureus infection activated TBK1/IRF3 pathway. IRF3 phosphorylation and IFN-α were attenuated in the presence of BX-795, amlexanox or IMD-0354, indicating that TBK1 and NF-κB were involved in S. aureus-induced IFN-α release. Collectively, S. aureus infection leads to TBK1-and NF-κB-dependent IFN-α production. It provides potential targets and theoretical basis for clinical prevention and treatment of S. aureus infection in the central nervous system.

Key words: Staphylococcus aureus, BV2, IFN-α, TBK1, IRF3

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