TNF-α and IL-10 Polymorphisms Increase the Risk to Hepatocellular Carcinoma in HCV Infected Individuals

被引:26
作者
Aroucha, Dayse Celia [1 ,2 ]
Carmo, Rodrigo Feliciano [3 ,4 ]
Silva Vasconcelos, Luydson Richardson [1 ,5 ]
Lima, Raul Emidio [6 ]
Mendonca, Taciana Furtado [4 ]
Arnez, Lucia Elena [7 ]
Mendonca Cavalcanti, Maria do Socorro [6 ]
Cartaxo Muniz, Maria Tereza [6 ]
Aroucha, Marcilio Lins [8 ]
Siqueira, Erika Rabelo [1 ]
Pereira, Luciano Beltrao [1 ]
Moura, Patricia [6 ]
Moreira Beltrao Pereira, Leila Maria [1 ,2 ]
Coelho, Maria Rosangela [9 ]
机构
[1] IFP, Recife, PE, Brazil
[2] Univ Pernambuco UPE, FCM, Recife, PE, Brazil
[3] Univ Fed Vale Sao Francisco UNIVASF, Colegiado Farm, Petrolina, Brazil
[4] Rede Nordeste Biotecnol RENORBIO, Recife, PE, Brazil
[5] Fundacao Oswaldo Cruz FIOCRUZ, Ctr Pesquisas Aggeu Magalhaes CPqAM, Dept Parasitol, Recife, PE, Brazil
[6] Univ Pernambuco UPE, ICB, Recife, PE, Brazil
[7] Fundacao Oswaldo Cruz FIOCRUZ, Inst Oswaldo Cruz, Lab Hanseniase, Rio De Janeiro, Brazil
[8] Univ Fed Pernambuco UFPE, CCS, Recife, PE, Brazil
[9] Univ Fed Pernambuco UFPE, LIKA, Setor Virol, Recife, PE, Brazil
关键词
interleukin; cytokines; inflammation; hepatitis c virus; HEPATITIS-C VIRUS; NECROSIS-FACTOR-ALPHA; INTERLEUKIN-10 GENE POLYMORPHISMS; ALLELE-SPECIFIC QUANTIFICATION; PROMOTER POLYMORPHISM; RHEUMATOID-ARTHRITIS; FUNCTIONAL-ANALYSIS; INTERFERON-GAMMA; LIVER-DISEASE; ASSOCIATION;
D O I
10.1002/jmv.24501
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Hepatitis C virus (HCV) is the major cause of hepatocellular carcinoma (HCC). The risk to develop HCC increases with the severity of liver inflammation and hepatic fibrosis. It is believed that a balance between the releases of pro-and anti-inflammatory cytokines will determine the clinical course of HCV and the risk to develop HCC. The inteleukin-10 (IL-10) and the tumor necrosis factor alpha (TNF-alpha) play key roles in the Th1 and Th2 balance during the inflammatory response against HCV. The aim of the present study was to investigate the association between polymorphisms in TNF-alpha -308 G>A (rs1800629), IL-10 -1082 G>A (rs1800896) and -819/-592 (rs1800871/rs1800872) with HCC risk in individuals with HCV. The present study evaluated 388 chronic HCV patients. Polymorphisms were determined by real-time PCR. Diplotypes associated with low IL-10 production and the TNF-alpha GG genotype were significantly associated with HCC occurrence after multivariate logistic regression analysis (P = 0.027 and P = 0.029, respectively). Additionally, the IL-10 -819 (-592) TT (AA) genotype was significantly associated with multiple nodules and HCC severity according to BCLC staging (P = 0.044 and P = 0.025, respectively). Patients carrying low production haplotypes of IL-10 and the TNF-alpha GG genotype have higher risk to develop HCC. (C) 2016 Wiley Periodicals, Inc.
引用
收藏
页码:1587 / 1595
页数:9
相关论文
共 65 条
[61]   Interleukin-10 gene polymorphisms and hepatocellular carcinoma susceptibility: A meta-analysis [J].
Wei, Yong-Gang ;
Liu, Fei ;
Li, Bo ;
Chen, Xi ;
Ma, Yu ;
Yan, Lv-Nan ;
Wen, Tian-Fu ;
Xu, Ming-Qing ;
Wang, Wen-Tao ;
Yang, Jia-Yin .
WORLD JOURNAL OF GASTROENTEROLOGY, 2011, 17 (34) :3941-3947
[62]   Natural history of hepatitis C [J].
Westbrook, Rachel H. ;
Dusheiko, Geoffrey .
JOURNAL OF HEPATOLOGY, 2014, 61 :S58-S68
[63]   Effects of a polymorphism in the human tumor necrosis factor alpha promoter on transcriptional activation [J].
Wilson, AG ;
Symons, JA ;
McDowell, TL ;
McDevitt, HO ;
Duff, GW .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (07) :3195-3199
[64]   Tumor necrosis factor gene polymorphisms in patients with cirrhosis from chronic hepatitis C virus infection [J].
Yee, LJ ;
Tang, J ;
Herrera, J ;
Kaslow, RA ;
van Leeuwen, DJ .
GENES AND IMMUNITY, 2000, 1 (06) :386-390
[65]   Tumor necrosis factor α promoter polymorphisms at position -: 308 in Taiwanese chronic hepatitis C patients treated with interferon-alpha [J].
Yu, ML ;
Dai, CY ;
Chiu, CC ;
Lee, LP ;
Lin, ZY ;
Chen, SC ;
Hsieh, MY ;
Wang, LY ;
Chen, CJ ;
Chuang, WL ;
Chang, WY .
ANTIVIRAL RESEARCH, 2003, 59 (01) :35-40