• 中文核心期刊
  • CSCD来源期刊
  • 中国科技核心期刊
  • CA、CABI、ZR收录期刊

留言板

尊敬的读者、作者、审稿人, 关于本刊的投稿、审稿、编辑和出版的任何问题, 您可以本页添加留言。我们将尽快给您答复。谢谢您的支持!

姓名
邮箱
手机号码
标题
留言内容
验证码

SOCS3负调控流感病毒诱导干扰素表达机理的初步研究

彭本群 胡精蕴 毛亚楠 王淑霖 王佳俊 陈梦颖 尤冬雪 王松

彭本群,胡精蕴,毛亚楠,等. SOCS3负调控流感病毒诱导干扰素表达机理的初步研究 [J]. 福建农业学报,2024,39(X):1−6
引用本文: 彭本群,胡精蕴,毛亚楠,等. SOCS3负调控流感病毒诱导干扰素表达机理的初步研究 [J]. 福建农业学报,2024,39(X):1−6
PENG B Q, HU J Y, MAO Y N, et al. Preliminary Research on the Mechanism of SOCS3 Negatively Regulating the Expression of Interferons Induced by Influenza Virus [J]. Fujian Journal of Agricultural Sciences,2024,39(X):1−6
Citation: PENG B Q, HU J Y, MAO Y N, et al. Preliminary Research on the Mechanism of SOCS3 Negatively Regulating the Expression of Interferons Induced by Influenza Virus [J]. Fujian Journal of Agricultural Sciences,2024,39(X):1−6

SOCS3负调控流感病毒诱导干扰素表达机理的初步研究

基金项目: 国家自然科学基金项目(U23A20235);福建省自然科学基金项目(2020J06016);福建农林大学科技创新专项基金(KFb22063XA)
详细信息
    作者简介:

    彭本群(1999 —),男,硕士研究生, 主要从事预防兽医学研究,E-mail:enjamin_Pong@outlook.com

    通讯作者:

    王松(1983 —),男,博士,教授,主要从事动物病原微生物与免疫学研究,E-mail:wscookie@163.com

  • 中图分类号: S852.65

Preliminary Research on the Mechanism of SOCS3 Negatively Regulating the Expression of Interferons Induced by Influenza Virus

  • 摘要:   目的  探究细胞因子信号转导抑制因子3(Suppressor of cytokine signaling 3, SOCS3)在流感病毒(Influenza virus)感染过程中对干扰素(Interferon, IFN)信号通路的调控作用。  方法  通过慢病毒感染的方式在人非小细胞肺癌细胞(A549细胞)中过表达SOCS3,利用siRNA技术在A549细胞中敲低SOCS3的表达,然后使用流感病毒感染SOCS3过表达或敲低的细胞系以及对照细胞系,于不同时间点收取RNA或蛋白样品,采用RT-PCR和Western blot技术检测干扰素信号通路中关键节点分子的表达或活化情况。  结果  检测发现细胞中过表达SOCS3后I型干扰素IFN-β和III型干扰素IL-28(Interleukin-28)、IL-29(Interleukin-29)表达水平下降,而敲低SOCS3表达后IFN-β及IL-28、IL-29的表达水平升高。进一步研究发现,过表达SOCS3对识别流感病毒RNA的模式识别受体视黄酸诱导基因-I(Retinoic acid-inducible gene 1, RIG-I)、黑色素瘤分化相关蛋白5(Melanoma differentiation-associated protein 5, MDA5)、Toll样受体3(Toll-like receptor 3, TLR3)以及干扰素调节因子7(Interferon regulatory factor 7, IRF7)的mRNA表达均有抑制作用。同时SOCS3还能影响干扰素下游信号转导与转录激活因子 1(Signal transducer and activator of transcription 1, STAT1)的活化,细胞中过表达SOCS3抑制流感病毒诱导的STAT1的磷酸化,而敲低SOCS3表达则使STAT1的磷酸化水平升高。  结论  流感病毒感染后,SOCS3能够在转录水平下调模式识别受体及干扰素调节因子的表达,抑制Ⅰ型和Ⅲ型干扰素的产生,同时还影响STAT1的活化从而阻断干扰素信号的传递。
  • 图  1  SOCS3抑制流感病毒感染后干扰素的产生

    Figure  1.  SOCS3 inhibits the production of interferons during influenza virus infection

    图  2  SOCS3抑制模式识别受体的表达

    Figure  2.  SOCS3 inhibits the expression of pattern recognition receptors

    图  3  SOCS3抑制IRF7的表达

    Figure  3.  SOCS3 inhibits the expression of IRF7

    图  4  SOCS3抑制流感病毒诱导的STAT1磷酸化

    Figure  4.  SOCS3 inhibits the phosphorylation of STAT1 induced by influenza virus infection

    表  1  RT-PCR引物序列

    Table  1.   Sequences of primers for RT-PCR

    引物
    Primer
    上游引物 5′-3′
    Forward primer 5′-3′
    下游引物 5′-3′
    Reverse primer 5′-3′
    GAPDH TGGGTGTGAACCATGAGAAGT AAGGCCATGCCAGTGAGCTT
    NP (Influenza virus) TCAAACGTGGGATCAATG GTGCAGACCGTGCTAAAA
    SOCS3 CAGTACGATGCCCCGCTTTA GAAGCTGGAGACTCAGGTGG
    IFN-β GCACTGGCTGGAATGAGACTA ACTCTGACTATGGTCCAGGCA
    IL-28 CCTGGTGGACGTCTTGGAC GCGGAAGAGGTTGAAGGTGA
    IL-29 TGGTGACTTTGGTGCTAGGC GGCCTTCTTGAAGCTCGCTA
    RIG-I GAAGATCCAGAATGCCAGAATC CTGGGATCTGATTCGCAAAA
    MDA5 CTGCTGCAGAAAACAATGGA TGGCTGAACTGTGGTTGAAA
    TLR3 AGTGCCGTCTATTTGCCACA GCATCCCAAAGGGCAAAAGG
    IRF3 GGGGAGTGATGAGCTACGTG CTACAATGAAGGGCCCCAGG
    IRF7 GAGCTGTGCTGGCGAGAAG CTCTCCAGGAGCCTTGGTTG
    下载: 导出CSV
  • [1] HUTCHINSON E C. Influenza virus [J]. Trends in Microbiology, 2018, 26(9): 809−810. doi: 10.1016/j.tim.2018.05.013
    [2] UYEKI T M, HUI D S, ZAMBON M, et al. Influenza [J]. Lancet, 2022, 400(10353): 693−706. doi: 10.1016/S0140-6736(22)00982-5
    [3] GORAYA M U, ZAIGHUM F, SAJJAD N, et al. Web of interferon stimulated antiviral factors to control the influenza A viruses replication [J]. Microbial Pathogenesis, 2020, 139: 103919. doi: 10.1016/j.micpath.2019.103919
    [4] WONG P T, GOFF P H, SUN R J, et al. Combined intranasal nanoemulsion and RIG-I activating RNA adjuvants enhance mucosal, humoral, and cellular immunity to influenza virus [J]. Molecular Pharmaceutics, 2021, 18(2): 679−698. doi: 10.1021/acs.molpharmaceut.0c00315
    [5] MA W, HUANG G, WANG Z, et al. IRF7: Role and regulation in immunity and autoimmunity [J]. Frontiers in Immunology, 2023, 14: 1236923. doi: 10.3389/fimmu.2023.1236923
    [6] YAO D D, BAO L L, LI F D, et al. H1N1 influenza virus dose dependent induction of dysregulated innate immune responses and STAT1/3 activation are associated with pulmonary immunopathological damage [J]. Virulence, 2022, 13(1): 1558−1572. doi: 10.1080/21505594.2022.2120951
    [7] HALLER O, KOCHS G. Mx genes: Host determinants controlling influenza virus infection and trans-species transmission [J]. Human Genetics, 2020, 139(6): 695−705.
    [8] 周斌, 万少兵, 王瑛, 等. SOCS3通过调控JAK2/STAT3信号通路改善急性肺损伤 [J]. 山西医科大学学报, 2023, 54(6):778−784.

    ZHOU B, WAN S B, WANG Y, et al. SOCS3 improves acute lung injury by regulating JAK2/STAT3 signaling pathway [J]. Journal of Shanxi Medical University, 2023, 54(6): 778−784. (in Chinese)
    [9] SIMS N A. The JAK1/STAT3/SOCS3 axis in bone development, physiology, and pathology [J]. Experimental & Molecular Medicine, 2020, 52: 1185−1197.
    [10] LIU S S, YAN R X, CHEN B, et al. Influenza virus-induced robust expression of SOCS3 contributes to excessive production of IL-6 [J]. Frontiers in Immunology, 2019, 10: 1843. doi: 10.3389/fimmu.2019.01843
    [11] SUN Y P, JIANG J W, PO T E, et al. IFN-λ: A new spotlight in innate immunity against influenza virus infection [J]. Protein & Cell, 2018, 9(10): 832−837.
    [12] BIONDO C, LENTINI G, BENINATI C, et al. The dual role of innate immunity during influenza [J]. Biomedical Journal, 2019, 42(1): 8−18. doi: 10.1016/j.bj.2018.12.009
    [13] HUANG B Z, CHEN H P, ZHENG Y B. MiR-103/miR-107 inhibits enterovirus 71 replication and facilitates type I interferon response by regulating SOCS3/STAT3 pathway [J]. Biotechnology Letters, 2021, 43(7): 1357−1369. doi: 10.1007/s10529-021-03115-z
    [14] YAKASS M B, FRANCO D, QUAYE O. Suppressors of cytokine signaling and protein inhibitors of activated signal transducer and activator of transcriptions As therapeutic targets in flavivirus infections [J]. Journal of Interferon & Cytokine Research, 2020, 40(1): 1−18.
    [15] LI L, WU H Y, LI Q M, et al. SOCS3-deficient lung epithelial cells uptaking neutrophil-derived SOCS3 worsens lung influenza infection [J]. Molecular Immunology, 2020, 125: 51−62. doi: 10.1016/j.molimm.2020.06.022
    [16] YANG H, DONG Y R, BIAN Y, et al. The influenza virus PB2 protein evades antiviral innate immunity by inhibiting JAK1/STAT signalling [J]. Nature Communications, 2022, 13: 6288. doi: 10.1038/s41467-022-33909-2
    [17] ZHANG Y L, XU L L, ZHANG Z, et al. Enterovirus D68 infection upregulates SOCS3 expression to inhibit JAK-STAT3 signaling and antagonize the innate interferon response of the host [J]. Virologica Sinica, 2023, 38(5): 755−766. doi: 10.1016/j.virs.2023.08.007
    [18] WANG X W, JIA Y Q, REN J, et al. Newcastle disease virus nonstructural V protein upregulates SOCS3 expression to facilitate viral replication depending on the MEK/ERK pathway [J]. Frontiers in Cellular and Infection Microbiology, 2019, 9: 317. doi: 10.3389/fcimb.2019.00317
    [19] XIE J Y, WANG M S, CHENG A C, et al. DHAV-1 inhibits type I interferon signaling to assist viral adaption by increasing the expression of SOCS3 [J]. Frontiers in Immunology, 2019, 10: 731. doi: 10.3389/fimmu.2019.00731
  • 加载中
图(4) / 表(1)
计量
  • 文章访问数:  37
  • HTML全文浏览量:  32
  • PDF下载量:  1
  • 被引次数: 0
出版历程
  • 收稿日期:  2024-01-03
  • 修回日期:  2024-02-29
  • 网络出版日期:  2024-03-28

目录

    /

    返回文章
    返回