本文選題：炎性小體 + 核苷酸結(jié)合寡聚化結(jié)構(gòu)域樣受體蛋白��； 參考：《暨南大學(xué)學(xué)報(自然科學(xué)與醫(yī)學(xué)版)》2017年04期

【摘要】：目的:探討乙肝病毒(HBV)是否激活了慢性乙型病毒性肝炎(CHB)患者外周血單個核細(xì)胞(PBMCs)內(nèi)核苷酸結(jié)合寡聚化結(jié)構(gòu)域樣受體蛋白3(NLRP3)、黑色素瘤缺乏因子2(AIM2)和干擾素誘導(dǎo)蛋白16(IFI16)炎癥小體,分析HBV影響炎癥小體活化的可能機(jī)制.方法:收集感染內(nèi)科臨床確診CHB患者35例.同時選取健康住院醫(yī)師28例為對照.以常規(guī)淋巴細(xì)胞分層液密度梯度離心法分離健康對照組和CHB患者組靜脈血得到PBMCs,采用逆轉(zhuǎn)錄、實(shí)時熒光定量PCR檢測CHB患者組和健康對照組PBMCs NLRP3、AIM2、IFI16、凋亡相關(guān)的斑點(diǎn)樣蛋白(ASC)、半胱天冬酶1(CASP1)、IL-1β、IL-18 mRNA表達(dá)水平,ELISA法檢測兩組血清中IL-1β蛋白分泌水平.結(jié)果:CHB患者組和健康對照組PBMCs ASC、NLRP3、AIM2、IL-1β、IL-18 mRNA表達(dá)水平及兩組血清IL-1β蛋白分泌水平無顯著性差異.CHB患者組PBMCs IFI16、CASP1 mRNA表達(dá)水平顯著上調(diào),且IFI16 mRNA表達(dá)水平與患者血清HBV DNA載量顯著正相關(guān)(r=0.699 8,P0.01).結(jié)論:慢性HBV感染未導(dǎo)致CHB患者PBMCs NLRP3、AIM2炎癥小體的活化;盡管HBV DNA可能誘導(dǎo)了CHB患者IFI16炎癥小體的高表達(dá),但通過抑制pro-caspase-1的活化、IL-1β的表達(dá),HBV阻斷了IFI16炎癥小體的活化效應(yīng).
[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.
【作者單位】： 暨南大學(xué)第二臨床醫(yī)學(xué)院深圳市人民醫(yī)院感染內(nèi)科;深圳市病原微生物重點(diǎn)實(shí)驗(yàn)室;暨南大學(xué)第二臨床醫(yī)學(xué)院深圳市人民醫(yī)院檢驗(yàn)科;
【基金】：廣東省深圳市科技創(chuàng)新委員會知識創(chuàng)新計劃基金項目(JCYJ20150403101028209)
【分類號】：R512.62

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