免疫因素在特发性门脉高压症发病机制中的作用  

Immune mechanism in pathogenesis of idiopathic portal hypertension

作　　者：王莉[1] 袁孟彪[1] 韩炜[1] 刘成霞[1] 

机构地区：[1]山东大学齐鲁医院消化内科,山东济南250012

出　　处：《山东大学学报（医学版）》2006年第6期583-585,589,共4页Journal of Shandong University:Health Sciences

基　　金：山东省自然科学基金资助课题(Y200016)

摘　　要：目的:探讨免疫因素在特发性门脉高压症(IPH)发病机制中的作用。方法:采用流式细胞术检测IPH和正常对照组外周血T淋巴细胞亚群和CD19+B细胞,IPH和肝硬化患者及正常对照组血清可溶性TNF-α受体-II(sTNF-αr-II)、可溶性血管细胞粘附分子-1(sVCAM-1)的水平及血管细胞粘附分子-1(VCAM-1)在肝脏中的表达。结果:与对照组相比,IPH组CD3+、CD4+、CD8+明显降低(P<0.05),CD4+/CD8+明显升高(P<0.05),CD19+无差别(P>0.05);IPH组血清中sTNF-αr-II和sVCAM-1水平明显高于对照组[(38.84±8.38)ng/ml vs(28.14±7.37)ng/ml;(44.06±17.28)ng/ml vs(32.18±8.72)ng/ml,P均<0.05],与肝硬化组无明显差异[(38.84±8.38)ng/ml vs(36.33±11.06)ng/ml;(44.06±17.28)ng/mlvs(34.78±11.32)ng/ml,P均>0.05];IPH组sTNF-和sVCAM-1水平呈正相关(r=0.556,P<0.05);VCAM-1在IPH和肝硬化患者的肝脏中均有明显的表达,但IPH患者在汇管区周围表达明显,而肝硬化患者表达散在,正常肝脏则几乎无表达。结论:IPH患者细胞免疫降低,在IPH发生中VCAM-1介导了炎症细胞对肝内门脉损伤,最终导致纤维化,sTNF-αr-II可独立也可通过上调VCAM-1表达起作用。Objective： To study the role of immune mechanism in the pathogenesis of idiopathic portal hypertension（IPH）. Methods： Subgroups of T and B lymphcyte were assyed by flow cytometric method. Serum levels of Soluble tumor necrosis factor-α receptor- Ⅱ （sTNF- r-Ⅱ） and soluble vascular cell adhesion molecule-1 （sVCAM-1） in IPH, normal and cirrhosis group were measured by ELISA method. And the expression of VCAM-1 in liver were detemrined in IPH, cirrhosis and nomral patients. Results： The prevalence of CD3^＋ , CD4^＋ and CD8^＋ in peripheral blood were significantly lower in the IPHs than in the healthy controls （ P 〈 0.05 ）, the ratio of CD4 ^＋/CD8 ^＋ was much higher in the IPHs than in the controls （ P 〈 0.05）, whereas there was no significant difference of CD19^＋ between the IPHs and the controls （ P 〉 0.05）. Expression of VCAM- 1 in the IPHs was found mainly in endothelial cells and sinusoidal lining cells around portal tracts, and scattered in sinusoidal lining cells in cirrhosis, whereas was not found in normal group. Serum levels of sVCAM-1 and sTNF-α r -Ⅱ increased in the IPHs compared with those in the controls [ （38.84 ± 8.38） ng/ml vs 28.14 ±7.37ng/ml; （44.06 ±17.28） ng/ml vs （ 32.18 ±8.72 ） ng/ml, （ P 〈 0.05） ]. In addition, TNFα- induced the up- regulation of VCAM-1（ r = 0.556, P 〈 0.05） in IPH. Conclusion：Cell immtme is lower in patients with IPH. VCAM-1 mediates interactions between lymphocytes and endothelial ceils of portal vessels in the pathogenesis of IPH. TNF-α induces the upregulation of VCAM-1, which may be a key cytokine involving in the histologic changes in the livers of IPH.

关 键 词：免疫 特发性门脉高压症 T淋巴细胞亚群 肿瘤坏死因子-Α 血管细胞粘附分子-1 

分 类 号：R575.2[医药卫生—消化系统]