NLRP3、AIM2、IFI16炎症小体在慢性乙型病毒性肝炎患者PBMC中的活化水平和与HBV感染的相关性分析

被引：11

作者：

陈洪涛 ^{[1
,2
]}

陈月 ^{[3
]}

吴诗品 ^{[1
]}

机构：

[1] 暨南大学第二临床医学院深圳市人民医院感染内科

[2] 深圳市病原微生物重点实验室

[3] 暨南大学第二临床医学院深圳市人民医院检验科

来源：

暨南大学学报(自然科学与医学版) | 2017年 / 38卷 / 04期

关键词：

炎性小体; 核苷酸结合寡聚化结构域样受体蛋白3; 黑素瘤缺乏因子2; 半胱天冬酶1; 干扰素诱导蛋白16; 乙型肝炎病毒;

D O I：

暂无

中图分类号：

R512.62 [];

学科分类号：

摘要：

目的:探讨乙肝病毒(HBV)是否激活了慢性乙型病毒性肝炎(CHB)患者外周血单个核细胞(PBMCs)内核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)、黑色素瘤缺乏因子2(AIM2)和干扰素诱导蛋白16(IFI16)炎症小体,分析HBV影响炎症小体活化的可能机制.方法:收集感染内科临床确诊CHB患者35例.同时选取健康住院医师28例为对照.以常规淋巴细胞分层液密度梯度离心法分离健康对照组和CHB患者组静脉血得到PBMCs,采用逆转录、实时荧光定量PCR检测CHB患者组和健康对照组PBMCs NLRP3、AIM2、IFI16、凋亡相关的斑点样蛋白(ASC)、半胱天冬酶1(CASP1)、IL-1β、IL-18 mRNA表达水平,ELISA法检测两组血清中IL-1β蛋白分泌水平.结果:CHB患者组和健康对照组PBMCs ASC、NLRP3、AIM2、IL-1β、IL-18 mRNA表达水平及两组血清IL-1β蛋白分泌水平无显著性差异.CHB患者组PBMCs IFI16、CASP1 mRNA表达水平显著上调,且IFI16 mRNA表达水平与患者血清HBV DNA载量显著正相关(r=0.699 8,P<0.01).结论:慢性HBV感染未导致CHB患者PBMCs NLRP3、AIM2炎症小体的活化;尽管HBV DNA可能诱导了CHB患者IFI16炎症小体的高表达,但通过抑制pro-caspase-1的活化、IL-1β的表达,HBV阻断了IFI16炎症小体的活化效应.

引用

页码：322 / 329

页数：8

共 7 条

[1] HBV inhibits LPS-induced NLRP3 inflammasome activation and IL-1β production via suppressing the NF-κB pathway and ROS production.[J].Xin Yu;Peixiang Lan;Xuben Hou;Qiuju Han;Nan Lu;Tao Li;Chenwei Jiao;Jian Zhang;Cai Zhang;Zhigang Tian.Journal of Hepatology.2016, 4
[2] BRCA1 Regulates IFI16 Mediated Nuclear Innate Sensing of Herpes Viral DNA and Subsequent Induction of the Innate Inflammasome and Interferon-β Responses.[J].Dipanjan Dutta;Sujoy Dutta;Mohanan Valiya Veettil;Arunava Roy;Mairaj Ahmed Ansari;Jawed Iqbal;Leela Chikoti;Binod Kumar;Karen E. Johnson;Bala Chandran.PLOS Pathogens.2015, 6
[3] Toll-like receptor-mediated immune responses are attenuated in the presence of high levels of hepatitis B virus surface antigen
Jiang, M.
Broering, R.
Trippler, M.
Poggenpohl, L.
Fiedler, M.
Gerken, G.
Lu, M.
Schlaak, J. F.
[J]. JOURNAL OF VIRAL HEPATITIS, 2014, 21 (12) : 860 - 872
[4] Interleukin-1 and Tumor Necrosis Factor-α Trigger Restriction of Hepatitis B Virus Infection via a Cytidine Deaminase Activation-induced Cytidine Deaminase (AID).[J].Koichi Watashi;Guoxin Liang;Masashi Iwamoto;Hiroyuki Marusawa;Nanako Uchida;Takuji Daito;Kouichi Kitamura;Masamichi Muramatsu;Hirofumi Ohashi;Tomoko Kiyohara;Ryosuke Suzuki;Jisu Li;Shuping Tong;Yasuhito Tanaka;Kazumoto Murata;Hideki Aizaki;Takaji Wakita.Journal of Biological Chemistry.2013, 44
[5] Constitutive Interferon-Inducible Protein 16-Inflammasome Activation during Epstein-Barr Virus Latency I, II, and III in B and Epithelial Cells
Ansari, Mairaj Ahmed
Singh, Vivek Vikram
Dutta, Sujoy
Veettil, Mohanan Valiya
Dutta, Dipanjan
Chikoti, Leela
Lu, Jie
Everly, David
Chandran, Bala
[J]. JOURNAL OF VIROLOGY, 2013, 87 (15) : 8606 - 8623
[6] IFI16 Acts as a Nuclear Pathogen Sensor to Induce the Inflammasome in Response to Kaposi Sarcoma-Associated Herpesvirus Infection
Kerur, Nagaraj
Veettil, Mohanan Valiya
Sharma-Walia, Neelam
Bottero, Virginie
Sadagopan, Sathish
Otageri, Pushpalatha
Chandran, Bala
[J]. CELL HOST & MICROBE, 2011, 9 (05) : 363 - 375
[7] The Inflammasome NLRs in Immunity; Inflammation; and Associated Diseases.[J].Beckley K. Davis;Haitao Wen;Jenny P.-Y. Ting.Annual Review of Immunology.2011, 1

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