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

发布时间：2018-05-18 15:25

本文选题：炎性小体 + 核苷酸结合寡聚化结构域样受体蛋白　；参考：《暨南大学学报(自然科学与医学版)》2017年04期

【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,P0.01).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.
[Abstract]:Objective: to investigate whether hepatitis B virus (HBV) activates the inflammatory corpuscles of nucleotide binding oligonucleotide domain like receptor protein 3nLRP3, melanoma deficiency factor 2AIM2) and interferon inducible protein 16 (IFI16) in peripheral blood mononuclear cells (PBMCs) of patients with chronic hepatitis B (CHB). To analyze the possible mechanism of HBV affecting the activation of inflammatory corpuscles. Methods: 35 patients with CHB were collected. At the same time, 28 healthy residents were selected as control group. PBMCs were isolated from venous blood of healthy control group and CHB group by conventional lymphocyte stratified liquid density gradient centrifugation. Real-time fluorescence quantitative PCR was used to detect the expression of PBMCs NLRP3AIM2 / IFI16, apoptosis-related dot-like protein (AsASCS) and cysteine asparaginase 1 (CASP1) and IL-1 尾 -IL-18 mRNA in the serum of CHB patients and healthy controls. The levels of IL-1 尾 secreted in serum of the two groups were detected by Elisa. Results there was no significant difference in the expression of PBMCs ASCNLRP3AIM2AIM2 尾 IL-18 mRNA and the level of serum IL-1 尾 protein secretion between the two groups. The expression of PBMCs IFI16, CASP1 mRNA in CHB patients was significantly up-regulated, and the expression of IFI16 mRNA was positively correlated with the serum HBV DNA load of the patients (P 0.01). Conclusion: chronic HBV infection did not induce the activation of PBMCs NLRP3AIM2 inflammatory bodies in CHB patients, although HBV DNA may induce the high expression of IFI16 inflammatory corpuscles in CHB patients, it blocked the activation of IFI16 inflammatory corpuscles by inhibiting pro-caspase-1 activation and IL-1 尾 expression.
【作者单位】：暨南大学第二临床医学院深圳市人民医院感染内科;深圳市病原微生物重点实验室;暨南大学第二临床医学院深圳市人民医院检验科;
【基金】：广东省深圳市科技创新委员会知识创新计划基金项目(JCYJ20150403101028209)
【分类号】：R512.62

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