期刊文献+

慢加急性乙型肝炎肝衰竭患者肝组织IFN-γ、TNF-α和IL-10的表达 被引量:7

Imbalanced intrahepatic expression of interferon gamma,tumor necrosis factor alpha,and interleukin-10 in hepatitis B virus infection patients with acute-on-chronic liver failure
下载PDF
导出
摘要 目的研究乙型肝炎慢加急性肝衰竭(ACLF)患者肝内促炎细胞因子和抗炎细胞因子的表达特性。方法采用免疫组化法检测乙型肝炎ACLF患者、慢性乙型肝炎患者和正常人肝组织IFN-γ、TNF-α和IL-10的表达。结果在ACLF患者肝组织IFN-γ和TNF-α阳性细胞数均明显高于慢性乙型肝炎患者和正常对照组(P均<0.001);ACLF患者、慢性乙型肝炎患者和正常人肝组织IL-10的表达无统计学差异(P>0.05);肝内IFN-γ表达与TNF-α具有明显的相关性(r=0.886,P<0.001)。结论乙型肝炎ACLF患者因肝内促炎细胞因子和抗炎细胞因子表达的失衡而发生了肝损伤。 Objectives This study attempted to determine intrahepatic expressions of proinflammatory and anti-inflammatory cytokines in patients with acute-on-chronic liver failure(ACLF)arosing from HBV infection.Methods In situ expressions of interferon(IFN-γ),tumor necrosis factor(TNF-α)and interleukin 10(IL-10)were analyzed in the livers of patients with ACLF,chronic hepatitis B(CHB),and normal controls(NC)by using immunohistochemistry.Results Intrahepatic IFN-γ and TNF-α expressions were markedly up-regulated in patients with ACLF as compared to CHB and NC(both P0.001);However,similar IL-10 expressions were observed in ACLF and CHB;IFN-γ over-expression was actively correlated with expression of TNF-α(r=0.886,P0.001).Conclusions The imbalanced expression of proinflammatory and anti-inflammatory cytokines may contribute to immuno-pathogenesis in HBV-infected ACLF.
机构地区 解放军第
出处 《实用肝脏病杂志》 CAS 2011年第2期116-118,共3页 Journal of Practical Hepatology
基金 国家自然科学基金资助项目(编号:81072424)
关键词 慢加急性肝衰竭I FN-γ TNF-αI L-10 免疫组化 Acute-on-chronic liver failure Interferon Tumor necrosis factor Interleukin-10 Immunohistochemistry
  • 相关文献

参考文献17

  • 1SEN S,WILLIAMS R,JALAN R. The pathophysiological basis of acute-on-chronic liver failure[J]. I~iver,2002,22 (suppl 2): 5-13. 被引量:1
  • 2JALAN R,WILLIAMS R. Acute-on-chronic liver failure: pathophysiological basis of therapeutic optlons[J]. Blood Purif, 2002,20:252-261. 被引量:1
  • 3WASMUTH HE,KUNZ D,YAGMUT E,et al. Patients with a- cute on chronic liver failure display'sepsis-like'immune paral- ysis[J]. Hepatology, 2005,42:195-201. 被引量:1
  • 4邹正升,陈菊梅,辛绍杰,邢汉前,李保森,李建宇,沈宏辉,刘艳萍.慢性重型病毒性肝炎发病特点的探讨[J].中华实验和临床病毒学杂志,2002,16(4):322-325. 被引量:9
  • 5王宇明,陈耀凯,顾长海,蒋黎,向德栋.重型肝炎命名和诊断分型的再认识──附477例临床分析[J].中华肝脏病杂志,2000,8(5):261-263. 被引量:78
  • 6ANDO K,MORIYAMA T,GUIDOTI'I LG,et al. Mechanisms of class I restricted immunopathology:A trangenic mouse model offulminant hepatitis[J]. Exp Med, 1993,178:1541-1554. 被引量:1
  • 7OHTA A,SEKIMOTO M,SATO M,et ai. Indispensable role for TNF-alpha and IFN-gamnm at the effector phase of liver in- jury mediated by Thl cells specific to hepatitis B virus sur-face antigen[J]. Immunology,2000,165:956-961. 被引量:1
  • 8ISHIDA Y,KONDO T,TSUNEYAMA K,et al.The pathogenic roles of tumor necrosis factor receptor p55 in acetaminophen- induced liver injury in mice[J]. Leukoc Biol,2004,75:59-67. 被引量:1
  • 9LOUIS H,LE MOINE O,PENY MO,et al. Production and role of interleukin-10 in concanavalin A-induced hepatitis inmice[J]. Hepatology, 1997,25:1382-1389. 被引量:1
  • 10DI MARCO R,XIANG M,ZACCONE P,et al. Concanavalin A-induced hepatitis in mice is prevented by interleukin (IL)- 10 and exacerbated by endogenous IL-10 deficiency[J]. Au- toimmunity, 1999,31:75-83. 被引量:1

二级参考文献13

共引文献2084

同被引文献64

引证文献7

二级引证文献45

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部