title: Interleukin-2 gene polymorphisms associated with increased risk of gastric atrophy from Helicobacter pylori infection.
abstract: BACKGROUND
  Gastric atrophy induced by Helicobacter pylori is thought to predispose patients to noncardiac gastric cancer development. However, the host genetic factors that influence the progression of gastric atrophy have not been elucidated. In this study, we examined the effects of cytokine polymorphisms on H. pylori-induced gastric atrophy.
  
  
  METHODS
  Blood samples were taken from 454 Japanese subjects. The interleukin-2 (IL-2; T-330G), IL-4 (C-33T), and IL-13 (C-1111T) polymorphisms were genotyped by polymerase chain reaction with confronting two-pair primers (PCR-CTPP). Anti-H. pylori IgG antibody and pepsinogen I and II were measured to diagnose H. pylori infection and atrophic gastritis.
  
  
  RESULTS
  The odds ratios (ORs) for the association between IL-2 polymorphism [OR = 2.78, 95% CI (confidence interval) = 1.26-6.17 (T/T to G/G)] or IL-4 polymorphism [OR = 2.22, 95% CI = 1.01-4.89 (T/C to C/C)] were increased significantly with gastric atrophy, whereas the corresponding OR of IL-13 polymorphism was decreased with gastric atrophy [OR = 0.61, 95% CI = 0.39-0.96 (C/T and T/T to C/C)]. There were no significant H. pylori seropositivity-related differences between these polymorphisms. We examined the relationship between these polymorphisms and gastric atrophy separately in H. pylori-seropositive and -seronegative groups. In the H. pylori-seropositive group, the IL-2 T/T (OR = 2.78, 95% CI = 1.12-6.93) had a significant association with gastric atrophy.
  
  
  CONCLUSIONS
  These results reveal that the IL-2 gene polymorphism is associated with an increased risk of gastric atrophy induced by H. pylori infection and might predispose to gastric cancer.
authors.affiliation: Department of Internal Medicine and Bioregulation, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
authors.forename: Shozo
authors.initials: S
authors.lastname: Togawa
authors.forename: Takashi
authors.initials: T
authors.lastname: Joh
authors.forename: Makoto
authors.initials: M
authors.lastname: Itoh
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Katsuda
authors.forename: Hidemi
authors.initials: H
authors.lastname: Ito
authors.forename: Keitaro
authors.initials: K
authors.lastname: Matsuo
authors.forename: Kazuo
authors.initials: K
authors.lastname: Tajima
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Hamajima
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D005260:Female; D005757:Gastritis, Atrophic / Q000235:genetics* / Q000382:microbiology; D020022:Genetic Predisposition to Disease; D016481:Helicobacter Infections / Q000382:microbiology*; D016480:Helicobacter pylori / Q000472:pathogenicity*; D006801:Humans; D018793:Interleukin-13 / Q000235:genetics / Q000378:metabolism; D007376:Interleukin-2 / Q000235:genetics* / Q000378:metabolism; D015847:Interleukin-4 / Q000235:genetics / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D012307:Risk Factors
chemical_list: D018793:Interleukin-13; D007376:Interleukin-2; D015847:Interleukin-4