Interleukin-1beta and -10 polymorphisms influence erosive reflux esophagitis and gastritis in Taiwanese patients.
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.
Cheng
Hsin-Hung
HH
Institute of Molecular and Cellular Biology and Department of Life Sciences, National Tsing Hua University, Hsinchu, Taiwan.
Chang
Chi-Sen
CS
Wang
Hung-Jung
HJ
Wang
Wen-Ching
WC
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
C508606:CXCL8 protein, human; C508609:IL10 protein, human; D053583:Interleukin-1beta; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10