title: Interleukin-1beta and -10 polymorphisms influence erosive reflux esophagitis and gastritis in Taiwanese patients.
abstract: OBJECTIVE
  Helicobacter pylori (H. pylori) infection induces cytokine production and is associated with gastrointestinal diseases. This study examined the relationship of gene polymorphisms, including interleukin (IL)-1beta, -10, -8, and tumor necrosis factor-alpha (TNF-alpha), H. pylori infection, and susceptibility to gastrointestinal disorders in Taiwanese patients.
  
  
  METHODS
  IL-1beta-511/-31/+3953, -10-1082/-819/-592, -8-251, and TNF-alpha-308 polymorphisms were assessed in 628 gastrointestinal disease patients, and 176 healthy controls were analyzed using the polymerase chain reaction-restriction fragment length polymorphism method.
  
  
  RESULTS
  IL-1beta-511 T/T and -31 C/C genotypes, and IL-1beta-511 T and -31 C alleles were associated with an increased risk of reflux esophagitis (P = 0.034, odds ratio [OR] = 1.384, 95% confidence interval [CI]: 1.023-1.871; P = 0.031, OR = 1.388, 95% CI: 1.028-1.873; P = 0.044, OR = 1.342, 95% CI: 1.008-1.786; and P = 0.040, OR = 1.349, 95% CI: 1.014-1.796, respectively). No relationship was found between H. pylori infection and the risk of reflux esophagitis. IL-10-819 C/T and -10-592 A/C genotypes and IL-10-1082/-819/-592 ATA/ACC and ATA/GCC haplotypes were associated with an increased risk of gastritis (P = 0.021, OR = 1.721, 95% CI: 1.084-2.733; P = 0.016, OR = 1.766, 95% CI: 1.112-2.805; P = 0.039, OR = 1.662, 95% CI: 1.024-2.697; and P = 0.035, OR = 1.600, 95% CI: 1.024-2.499, respectively).
  
  
  CONCLUSIONS
  Among Taiwanese patients, IL-1beta and -10 polymorphisms were associated with an increased risk of erosive reflux esophagitis and gastritis, respectively.
authors.affiliation: Institute of Molecular and Cellular Biology and Department of Life Sciences, National Tsing Hua University, Hsinchu, Taiwan.
authors.forename: Hsin-Hung
authors.initials: HH
authors.lastname: Cheng
authors.forename: Chi-Sen
authors.initials: CS
authors.lastname: Chang
authors.forename: Hung-Jung
authors.initials: HJ
authors.lastname: Wang
authors.forename: Wen-Ching
authors.initials: WC
authors.lastname: Wang
mesh_terms: D000328:Adult; D044466:Asian People / Q000235:genetics*; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D004942:Esophagitis, Peptic / Q000208:ethnology / Q000235:genetics* / Q000276:immunology / Q000382:microbiology; D005260:Female; D005756:Gastritis / Q000208:ethnology / Q000235:genetics* / Q000276:immunology / Q000382:microbiology; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D006239:Haplotypes; D016481:Helicobacter Infections / Q000208:ethnology; D016480:Helicobacter pylori / Q000472:pathogenicity; D006801:Humans; D016753:Interleukin-10 / Q000235:genetics*; D053583:Interleukin-1beta / Q000235:genetics*; D016209:Interleukin-8 / Q000235:genetics; D015810:Linkage Disequilibrium; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D011110:Polymorphism, Genetic; D018570:Risk Assessment; D012307:Risk Factors; D013624:Taiwan / Q000453:epidemiology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: C508606:CXCL8 protein, human; C508609:IL10 protein, human; D053583:Interleukin-1beta; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10