粒-巨噬细胞集落刺激因子在乙型肝炎肝损害中的作用

Role of Granulocyte-macrophage Colony Stimulating Factor in Injury of Hepatitis B

为探讨粒 -巨噬细胞集落刺激因子 (GM- CSF)在乙型肝炎肝损害过程中的意义及其与肿瘤坏死因子 (TNF-α)和内毒素之间可能存在的关系 ,应用酶联免疫吸附试验 (EL ISA)同期检测了 73例乙型肝炎患者及 12例健康献血员 GM- CSF和 TNF水平 ,并用改良的鲎变形裂解产物 -鲎试剂与合成基质的偶氮显色法 (L AL)测定其血清内毒素水平。实验结果显示 :在不同类型的乙型肝炎患者中 ,与对照组相比 ,肝硬化、重症肝炎与慢性肝炎中重度组的血清 GM-CSF水平升高 (P<0 .0 5 ) ,而慢性肝炎轻度组 ,血清 GM- CSF水平与对照组相比无显著差异 (P>0 .0 5 )。在重症肝炎组中 ,血清 GM- CSF水平与 TNF- α水平和内毒素水平均呈显著正相关 (r=0 .4 36 9,0 .5 70 5 ) ,而与血清白蛋白水平呈负相关 (r=- 0 .4 0 72 ,P<0 .0 5 ) ;在慢性肝炎中重度组中 ,血清 GM- CSF与丙氨酸转氨酶水平呈正相关 (r=0 .6 0 6 0 ,P<0 .0 5 ) ;在肝硬化组中 ,GM- CSF与血清白蛋白水平呈负相关 (r=- 0 .5 137,P<0 .0 5 )。提示 :1GM- CSF在慢性乙型肝炎肝损害中可能起到免疫激活作用 ,通过激活免疫反应特别是细胞免疫反应 ,间接造成肝细胞的损害 ;2 GM-CSF与重症乙型肝炎发病关系密切 ,其机制可能与内毒素血症有关 ;3GM- CSF可能在乙型肝炎肝硬化的发生?

The role of granulocyte macrophage colony stimulating factor (GM CSF), tumor necrosis factor (TNF) and endotoxin (ET) in the pathogenesis of chronic and severe hepatitis (SH) and possible relationship between them were investigated. GM CSF and TNFα were measured by ELISA in sera of 73 patients with hepatitis B and 12 healthy blood donors. At same time, serum ET was measured by limulus amebocyte lysate test (LAL). It was found that the serum level of GM CSF was elevated in the patients with cirrhosis, SH and moderate and serious chronic hepatitis (CH) as compared with controls respectively ( P <0 05). While in the patients with mild CH, there was no significant difference in serum GM CSF as compared with controls. In the patients with SH, a significantly positive correlation between GM CSF and TNFα (r=0 4369, P <0 05) or ET ( r=0 5705, P <0 01) was observed, and a markedly negative correlation between GM CSF and albumin ( r=-0 4072, P<0 05 ) was found. In the patients with moderate and serious CH, there was a positive correlation between GM CSF and alkaline transaminase ( r=0 6060, P <0 05). In the patients with cirrhosis, a significantly negtive correlation between GM CSF and albumin ( r =-0 5137) existed. These results suggested GM CSF may be involved in the pathogenesis of SH, which is possibly related to endotoxmia; In CH, GM CSF may indirectly injury hepatocytes through activating immune response, especially cellular immune reaction; GM CSF may play a certain role in the progress of cirrhisis.