title: Polymorphisms of interleukin-1beta in Japanese patients with hepatitis B virus infection.
abstract: OBJECTIVE
  Hepatitis B virus (HBV) induces liver cirrhosis (LC) and hepatocellular carcinoma (HCC) mainly by causing chronic necro-inflammatory hepatic disease. Our aim was to investigate the relationships between the polymorphisms of the interleukin-1B (IL-1B) promoter region and the interleukin-1 receptor antagonist gene (IL-1RN) and disease progression in an HBV-infected Japanese population.
  
  
  METHODS
  Genomic DNA was extracted from the peripheral blood of 237 HBV carriers. Polymorphisms in IL-1B and IL-1RN were analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and PCR with confronting two-pair primers (PCR-CTPP) methods. These polymorphic sites include the promoter regions of IL-1B at positions -511 and -31, and IL-1RN variable tandem repeats.
  
  
  RESULTS
  The IL-1B -31 and -511 loci were in complete linkage disequilibrium, and the frequency of the IL-1B -31 T carrier (IL-1B -31 T/T or T/C) was significantly higher in HBV carriers with LC compared to those without LC (LC; 86.1% vs non-LC; 72.1%, P=0.009). There was no difference in the genotype distribution of the IL-1RN polymorphism.
  
  
  CONCLUSIONS
  This is the first report describing the association between IL-1B polymorphism and HBV-related hepatic fibrosis, and our data suggest that IL-1B polymorphisms may be related to disease progression of HBV-related hepatitis in Japan.
authors.affiliation: Clinical Research Center, National Nagasaki Medical Center, Kubara 2-1001-1, Omura 856-8562, Japan. migita@nmc.hosp.go.jp
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Migita
authors.forename: Yumi
authors.initials: Y
authors.lastname: Maeda
authors.forename: Seigo
authors.initials: S
authors.lastname: Abiru
authors.forename: Minoru
authors.initials: M
authors.lastname: Nakamura
authors.forename: Atsumasa
authors.initials: A
authors.lastname: Komori
authors.forename: Seiji
authors.initials: S
authors.lastname: Miyazoe
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Nakao
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Yatsuhashi
authors.forename: Katsumi
authors.initials: K
authors.lastname: Eguchi
authors.forename: Hiromi
authors.initials: H
authors.lastname: Ishibashi
mesh_terms: D000328:Adult; D000368:Aged; D018450:Disease Progression; D005260:Female; D016679:Genome, Viral / Q000235:genetics; D006509:Hepatitis B / Q000208:ethnology / Q000209:etiology / Q000235:genetics* / Q000503:physiopathology; D006515:Hepatitis B virus / Q000235:genetics*; D006801:Humans; D053583:Interleukin-1beta / Q000235:genetics*; D007564:Japan; D008103:Liver Cirrhosis / Q000209:etiology / Q000503:physiopathology / Q000821:virology; D008297:Male; D008875:Middle Aged; D012150:Polymorphism, Restriction Fragment Length; D011401:Promoter Regions, Genetic / Q000235:genetics / Q000502:physiology; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors / Q000235:genetics; D012307:Risk Factors
chemical_list: D053583:Interleukin-1beta; D017472:Receptors, Interleukin-1