title: H. pylori genotypes and cytokine gene polymorphisms influence the development of gastric intestinal metaplasia in a Chinese population.
abstract: BACKGROUND
  Cytokine gene polymorphisms and Helicobacter pylori (HP) genotypes have been linked to gastric cancer development in Western countries. We determined the role of host cytokine polymorphisms and bacterial virulent factors in the development of gastric intestinal metaplasia (IM) in a Chinese population with a high background gastric cancer incidence.
  
  
  METHODS
  Three hundred two HP-infected noncancer individuals living in Shandong province of China with available DNA were studied. Polymorphisms in different loci of inflammatory cytokines Interleukin IL-1B, IL-1RN, Interleukin IL-8, IL-10, IL-18, tumor necrosis factor-A (TNF-A), and Transforming growth factor (TGF-B), were determined by allelic discriminating TaqMan polymerase chain reaction (PCR) or a variable number of tandem repeats. Presence of HP virulence factors in cagA, vacA, and babA2 were determined by PCR. Baseline gastric biopsies were assessed for the presence of IM.
  
  
  RESULTS
  Among HP-infected subjects, carriers of the IL-1B-511 T allele were associated with a modestly greater prevalence of IM (adjusted OR 2.0, 95% CI 1.0-3.7). There was no association between the presence of IM and polymorphisms in other inflammatory cytokines. Although most subjects from this region harbored the virulent HP strains, carriage of the vacA m1 strain was associated with a significantly higher prevalence of IM (adjusted OR 1.8, 1.1-3.0). The presence of both host (IL-1B-511 T) and HP (vacA m1) genotypes further increased the risk of IM (OR 5.7, 2.0-16) when compared with individuals with the low-risk genotype.
  
  
  CONCLUSIONS
  The carriage of proinflammatory IL-1B-511 and HP vacA m1 genotypes was associated with the development of gastric IM in the Chinese.
authors.affiliation: Institute of Digestive Disease, Faculty of Medicine, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong SAR.
authors.forename: Wai K
authors.initials: WK
authors.lastname: Leung
authors.forename: Martin C W
authors.initials: MC
authors.lastname: Chan
authors.forename: Ka-Fai
authors.initials: KF
authors.lastname: To
authors.forename: Ellen P S
authors.initials: EP
authors.lastname: Man
authors.forename: Enders K W
authors.initials: EK
authors.lastname: Ng
authors.forename: Eagle S H
authors.initials: ES
authors.lastname: Chu
authors.forename: James Y W
authors.initials: JY
authors.lastname: Lau
authors.forename: San-ren
authors.initials: SR
authors.lastname: Lin
authors.forename: Joseph J Y
authors.initials: JJ
authors.lastname: Sung
mesh_terms: D002681:China; D016207:Cytokines / Q000235:genetics*; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology / Q000821:virology; D005814:Genes, Viral; D005838:Genotype; D016481:Helicobacter Infections / Q000473:pathology; D016480:Helicobacter pylori / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D007378:Interleukins / Q000235:genetics; D008297:Male; D008679:Metaplasia; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D011230:Precancerous Conditions / Q000235:genetics* / Q000473:pathology / Q000821:virology*; D013274:Stomach Neoplasms / Q000235:genetics* / Q000473:pathology / Q000821:virology*; D016212:Transforming Growth Factor beta / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics; D037521:Virulence Factors / Q000378:metabolism
chemical_list: D016207:Cytokines; D007378:Interleukins; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D037521:Virulence Factors