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山东大学学报(医学版)

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黑素瘤缺乏因子2诱导的固有免疫在慢性乙型肝炎发病机制中的作用

潘家超1,2,张乐1,2, 徐琳琳3,单晓宇2,杜文军2,陈士俊2   

  1. 1.山东大学医学院, 山东 济南 250012; 2.济南市传染病医院介入治疗中心, 山东 济南 250021;
    3. 济南市传染病医院科教科, 山东 济南 250021
  • 收稿日期:2013-11-05 出版日期:2014-04-10 发布日期:2014-04-10
  • 通讯作者: 陈士俊 E-mail:csj7516@sina.com
  • 基金资助:
    山东省科技厅资助项目(2011GSF12111)

Role of innate immunity induced by AIM2 in the pathogenesis of chronic hepatitis B

PAN Jiachao1,2, ZHANG Le1,2, XU Linlin3, SHAN Xiaoyu2, DU Wenjun2, CHEN Shijun2   

  1. 1. School of Medicine, Shandong University, Jinan 250012, Shandong, China;
    2. Interventional Therapy Center for Liver Tumor, Jinan Infectious Disease Hospital, Jinan 250021, Shandong,  China;
    3. Department of Science and Education, Jinan Infectious Disease Hospital, Jinan 250021, Shandong, China
  • Received:2013-11-05 Online:2014-04-10 Published:2014-04-10

摘要: 目的  初步探讨黑素瘤缺乏因子2(AIM2)诱导的固有免疫在慢性乙型肝炎(CHB)发病机制中的作用。方法  47例慢性乙型肝炎患者为实验组,23例脂肪肝患者为对照组,采用免疫组织化学法分别测定两组患者肝组织中AIM2、Caspase-1、IL-1β及IL-18的表达,组间比较采用χ2检验,相关性分析采用Spearman相关分析。结果  实验组患者肝组织中AIM2的表达阳性率(89.3%)明显高于对照组(43.5%)(χ2=15.655,P<0.01),实验组AIM2的表达强度与Caspase-1呈正相关(rs=0.738, P<0.01),IL-1β和IL-18的表达强度与AIM2的表达强度呈正相关(rs=0.527, 0.642, P<0.01)。ALT和AST的水平与AIM2表达强度呈正相关(rs=0.325,0.362,P<0.01)。高病毒载量组(HBV-DNA≥1×105copies/mL)AIM2的表达强度高于低病毒载量组(HBV-DNA<1×105copies/mL)(χ2=27.572,P<0.01)。结论  AIM2可以结合HBV-DNA,通过Caspase-1途径激活固有免疫,引起炎性因子IL-1β、IL-18的释放,导致慢性乙型肝炎炎症的发生。

关键词: 黑素瘤缺乏因子-2;慢性乙型肝炎;半胱天冬酶-1;白介素1&beta, ;白介素18

Abstract: Objective  To explore the role of innate immunity induced by absent in melanoma 2 (AIM2) in the pathogenesis of chronic hepatitis B (CHB). Methods  A total of 70 cases were enrolled in this study, including 47 CHB cases as the experimental group and 23 cases of fatty liver as the controls group. The immunohistochemical method was adopted to detect the expressions of AIM2, Caspase-1, IL-1β and IL-18 in liver tissues. The differences between the two groups were compared with chi-square test, and the correlation was analyzed using spearman test. Results  The positive rate of AIM2 expression in the experimental group (89.3%) was significantly higher than  that in the control group (43.5%) (χ2 = 15.655, P<0.01). In the experimental group, Caspase-1 was positively correlated with AIM2 (rs=0.738, P<0.01); IL-1β and IL-18 were positively correlated with AIM2 (rs=0.527, 0.642, P<0.01). ALT and AST were positively correlated with AIM2 (rs = 0.325, 0.362, P<0.01). The AIM2 expression in the high HBV titers group (HBV-DNA ≥ 1×105 copies/mL) was significantly higher than that in the low HBV titers group (HBV-DNA < 1×105 copies/ml)(χ2= 27.572, P<0.01). Conclusion  In the innate immune response to HBV infection, AIM2 can recognize HBV-DNA, activate Caspase-1 pathways subsequently, release IL-1β and IL-18 inflammatory factors, thus leading to liver inflammatory damages in chronic hepatitis B.

Key words: Absent in melanoma 2, Chronic hepatitis B, Interleukin-1β, Interleukin-18, Caspase-1

中图分类号: 

  • R574
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