Impact of serum levels and gene polymorphism of cytokines on chronic hepatitis C infection

被引:50
作者
Chen, Tzy-Yen
Hsieh, Yih-Shou
Wu, Triang-Tiau
Yang, Shun-Fa
Wu, Chia-Jun
Tsay, Gregory J.
Chiou, Hui-Ling
机构
[1] Chung Shan Med Univ, Sch Med Lab & Biotechnol, Sect 1, Taichung, Taiwan
[2] Chung Shan Med Univ, Inst Biochem & Biotechnol, Inst Med, Taichung, Taiwan
[3] Chung Shan Med Univ Hosp, Dept Internal Med, Taichung, Taiwan
[4] Chung Shan Med Univ Hosp, Dept Clin Lab, Taichung, Taiwan
关键词
D O I
10.1016/j.trsl.2007.01.007
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
The factors leading to clearance or persistent infection of hepatitis C virus (HCV) were not well defined, and the importance of the host immune response has been highlighted. Therefore, the impact of the serum concentration and genetic polymorphism of several cytokines on the outcome of HCV infection warrant additional study. Enzyme-linked immunosorbent assay was employed to measure serum tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-4, and IL- 10 concentrations on 72 hepatitis C patients and 180 controls. Furthermore, the association between single nucleotide polymorphism (SNP) of genes of these cytokines and hepatitis C infection was evaluated by polymerase chain reaction- restriction fragment length polymorphism and statistical analysis. These analyzed SNPs of cytokines included TNF-alpha G238A, TNF-alpha G308A, IL-4 C589T, IL-10 A1082G, IL-10 T819C, and IL-10 A592C. Serum levels of TNF-mu alpha, IL-4, and IL-10 were significantly higher in hepatitis C patients than that of controls (P < 0.001). Furthermore, the distribution of TNF-alpha G308A genotypes and alleles, but not others, was statistically different between patients and controls (P < 0.05). These data suggested the distribution of polymorphism at TNF-alpha G308A may be different between normal subjects and patients with chronic infection of hepatitis C.
引用
收藏
页码:116 / 121
页数:6
相关论文
共 35 条
[1]   CA repeat allele polymorphism in the first intron of the human interferon-γ gene is associated with lung allograft fibrosis [J].
Awad, M ;
Pravica, V ;
Perrey, C ;
El Gamel, A ;
Yonan, N ;
Sinnott, PJ ;
Hutchinson, IV .
HUMAN IMMUNOLOGY, 1999, 60 (04) :343-346
[2]   Genotypic variation in the transforming growth factor-β1 gene -: Association with transforming growth factor-pi production, fibrotic lung disease, and graft fibrosis after lung transplantation [J].
Awad, MR ;
El-Gamel, A ;
Hasleton, P ;
Turner, DM ;
Sinnott, PJ ;
Hutchinson, IV .
TRANSPLANTATION, 1998, 66 (08) :1014-1020
[3]   Association of the HLA-DRB1*01 allele with spontaneous viral clearance in an Irish cohort infected with hepatitis C virus via contaminated anti-D immunoglobulin [J].
Barrett, S ;
Ryan, E ;
Crowe, J .
JOURNAL OF HEPATOLOGY, 1999, 30 (06) :979-983
[4]   The natural course of hepatitis C virus infection after 22 years in a unique homogenous cohort: spontaneous viral clearance and chronic HCV infection [J].
Barrett, S ;
Goh, J ;
Coughlan, B ;
Ryan, E ;
Stewart, S ;
Cockram, A ;
O'Keane, JC ;
Crowe, J .
GUT, 2001, 49 (03) :423-430
[5]   Pathogenesis, diagnosis and management of hepatitis C [J].
Boyer, N ;
Marcellin, P .
JOURNAL OF HEPATOLOGY, 2000, 32 :98-112
[6]   Immunoregulatory cytokines in chronic hepatitis C virus infection: Pre- and posttreatment with interferon alfa [J].
Cacciarelli, TV ;
Martinez, OM ;
Gish, RG ;
Villanueva, JC ;
Krams, SM .
HEPATOLOGY, 1996, 24 (01) :6-9
[7]   Tumor necrosis factor-α promoter polymorphism at position-308 predicts response to combination therapy in hepatitis C virus infection [J].
Dai, CY ;
Chuang, WL ;
Chang, WY ;
Chen, SC ;
Lee, LP ;
Hsieh, MY ;
Hou, NJ ;
Lin, ZY ;
Huang, JF ;
Hsieh, MY ;
Wang, LY ;
Yu, ML .
JOURNAL OF INFECTIOUS DISEASES, 2006, 193 (01) :98-101
[8]  
FERRARI C, 1994, HEPATOLOGY, V19, P286
[9]   The effect of novel polymorphisms in the interleukin-6 (IL-6) gene on IL-6 transcription and plasma IL-6 levels, and an association with systemic-onset juvenile chronic arthritis [J].
Fishman, D ;
Faulds, G ;
Jeffery, R ;
Mohamed-Ali, V ;
Yudkin, JS ;
Humphries, S ;
Woo, P .
JOURNAL OF CLINICAL INVESTIGATION, 1998, 102 (07) :1369-1376
[10]  
Höhler T, 1998, CLIN EXP IMMUNOL, V111, P579