摘要
目的 探讨Th1/Th2细胞因子在乙型肝炎发病机制中的意义。方法 采集 7例急性病毒性肝炎、12例慢性乙型肝炎、10例慢性重型乙型肝炎患者和 10例健康献血员血清 ;分离 15例慢性乙型肝炎、14例慢性重型乙型肝炎和 10例健康献血员PBMC ,在PHA P刺激下培养 72h ,收取培养上清。采用双抗体夹心ELISA法检测血清和PBMC培养上清IL 2与IL 10水平。结果 急性肝炎血清IL 2高于正常对照 (P <0 .0 1)、高于慢性乙型肝炎 (P <0 .0 5 )、高于慢性重型乙型肝炎 (P <0 .0 5 )。慢性重型乙型肝炎血清IL 2高于正常对照 (P <0 .0 1) ,慢性重型乙型肝炎PBMC培养上清IL 2高于正常对照 (P <0 .0 5 )。血清IL 2与ALT呈正相关 (P <0 .0 1) ,PBMC培养上清IL 2与ALT呈正相关 (P <0 .0 5 )。血清IL 10与PBMC培养上清IL 10与ALT无相关性 ,血清IL 2与IL 10呈正相关 (P <0 .0 1)。结论 Th1型细胞因子IL 2上调与乙型肝炎肝脏的炎症活动相关 ,IL 2的分泌低下可能造成细胞免疫力低下 ,与HBV的持续感染有关。IL 10可能作为IL 2的拮抗因子随IL 2分泌增加而升高。
Objective To explore the significance of Th1/Th2 cytokines in the pathogenesis of hepatitis B. Methods Sera were collected from 7 patients with acute hepatitis,12 chronic hepatitis B,10 chronic severe hepatitis B and 10 healthy blood donors.PBMCs from 15 patients with chronic hepatitis B , 14 chronic severe hepatitis B and 10 healthy blood donors were cultured with PHA P in vitro . The supernatant of PBMCs culture was collected 72 h after incubation.Then the level of IL 2 and IL 10 in sera and supernatant were measured by ELASA method respectively. Results The level of IL 2 was higher in sera of acute hepatitis than in healthy blood donors( P <0.01), than in chronic hepatitis B( P < 0.05) and than in chronic severe hepatitis B( P <0.05). The level of IL 2 was higher in sera of chronic severe hepatitis B than in healthy blood donors( P <0.01). The level of IL 2 was higher in PBMC supernatant of chronic severe hepatitis B than in control group( P <0.05). The level of IL 2 in sera positively correlated with ALT( P <0.01). The level of IL 2 in PBMC supernatant positively correlated with ALT( P <0.05). The level of IL 10 in sera and in PBMC supernatant did not correlate with ALT . The level of IL 10 in sera positively correlated with IL 2 in sera ( P <0.01). Conclusion The increase of IL 2 (Th1 cytokine) relates to active inflammation in liver of hepatitis B. The decrease of IL 2 may induce the decrease of cellular immunity and HBV persistent infection. IL 10 may be as an antagonistic cytokine of IL 2 is increased with the increase of IL 2.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2001年第11期1324-1326,共3页
Journal of Third Military Medical University