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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。
Objective To investigate the role of innate immunity mediated by melanoma deficiency factor 2 (AIM2) in the pathogenesis of chronic hepatitis B (CHB). Methods 47 cases of chronic hepatitis B patients were experimental group and 23 cases of fatty liver patients as control group. The expression of AIM2, Caspase-1, IL-1β and IL-18 in liver tissue of two groups were detected by immunohistochemical method, Chi-square test was used to compare between groups, and Spearman correlation analysis was used to analyze the correlation. Results The positive expression rate of AIM2 in experimental group was significantly higher than that in control group (89.3%, 43.5%, χ2 = 15.655, P <0.01). The positive expression of AIM2 in experimental group was positively correlated with Caspase- 0.738, P <0.01). The expressions of IL-1β and IL-18 were positively correlated with the expression of AIM2 (rs = 0.527,0.642, P <0.01). The levels of ALT and AST were positively correlated with the expression of AIM2 (rs = 0.325,0.362, P <0.01). The expression level of AIM2 in high viral load group (HBV-DNA≥1 × 105copies / mL) was higher than that in low virus load group (HBV-DNA <1 × 105copies / mL) (χ2 = 27.572, P <0.01). Conclusion AIM2 can bind to HBV-DNA and activate innate immunity through Caspase-1 pathway, which can cause the release of inflammatory factors IL-1β and IL-18, leading to the occurrence of chronic hepatitis B inflammation.