【摘要】 目的:了解乙型肝炎病毒(HBV)慢性感染患者外周血单个核细胞(PBMC)中CXCR1、CXCR2及IL-8 mRNA表达水平及与α干扰素(IFN-α)治疗的关系。方法:采用实时定量PCR法动态观察30例慢性乙型肝炎患者接受IFN-α治疗前、治疗3个月、6个月后其外周血单个核细胞CXCR1、CXCR2及IL-8 mRNA表达水平。结果:治疗前慢性乙肝患者CXCR1、CXCR2及IL-8 mRNA表达水平分别为(0.44740.0386)、(0.4720 0.0458)、(1.1897 0.1028),均高于正常对照组(n=36),其中CXCR1及IL-8 mRNA水平升高显著,差异有统计学意义(P<0.01)。治疗过程中CXCR1、CXCR2及IL-8表达水平均显著下降。IFN-α治疗6个月后CXCR1、CXCR2及IL-8 mRNA表达水平分别为(0.41290.0395)、(0.4461 0.0477)、(0.8660 0.1307),与治疗前相比,差异有显著性(P<0.01或P<0.05)。治疗前的CX-CR1、CXCR2及IL-8的表达水平在HBV高复制组(HBV-DNA>106,n=22)明显高于HBV低复制组(HBV-DNA<106,n=8),差异有统计学意义(P<0.05)。结论:慢性乙肝患者外周血单个核细胞中CXCR1和IL-8表达水平显著升高,在干扰素治疗后,其表达水平下调,证明其可能与慢性乙肝炎症的发生机制相关。更多还原

【Abstract】 AIM: To study the mRNA levels of chemokine receptor CXCR1,CXCR2 and IL-8 in the patients with chronic hepatitis B and their association with IFN therapy.METHODS: The mRNA levels of CXCR1,CXCR2 and IL-8 in peripheral blood mononuclear cells(PBMC)of chronic hepatitis B patients were determined by real-time RT-PCR before and during the IFN-α therapy.RESULTS: The mRNA levels of CXCR1(0.4474±0.0386)and IL-8(1.1897±0.1028)in peripheral blood of the patients with chronic hepatitis B were significantly higher than those in healthy donors(P<0.01).The mRNA level of CXCR2(0.4720±0.0458)was higher than those in healthy donors,but there was no significant differences between the two groups.During the treatment,the mRNA levels of CXCR1,CXCR2 and IL-8 obviously decreased.After treatment for six month,the mRNA level of CXCR1(0.4129±0.0395),CXCR2(0.4461±0.0477) and IL-8(0.8660±0.1307)were significantly lower than those before treatment(P<0.01 or P<0.05).Additionally,the expressive levels of CXCR1,CXCR2 and IL-8 in the high HBV loading group(HBV-DNA>106)were much higher than those in the low HBV loading group(HBV-DNA<106).CONCLUSION: CXCR1 and IL-8 may contribute to hepatic inflammation.Among them,CXCR1,CXCR2 and IL-8 decrease after IFN treatment,which illustrates that IFN-α plays an important role in down-regulating inflammation response,controlling the development of the patients’ condition.更多还原