title: Aberrant CpG island hypermethylation in pediatric gastric mucosa in association with Helicobacter pylori infection.
abstract: BACKGROUND
  Helicobacter pylori infection is primarily acquired during childhood and persists throughout life in the absence of eradication with antibiotics. Helicobacter pylori infection induces methylation in the promoter CpG island loci in gastric epithelial cells. Thus, aberrant CpG island hypermethylation in gastric epithelial cells likely occurs early in life, although there are no existing data supporting this notion.
  
  
  OBJECTIVE
  To identify whether aberrant CpG island hypermethylation occurs in pediatric stomach mucosa in association with H pylori infection and to compare methylation profiles of samples from pediatric and adult stomach tissues.
  
  
  METHODS
  We analyzed pediatric (n = 47) and adult (n = 38) gastric mucosa samples for their methylation status in 12 promoter CpG island loci using the MethyLight assay and compared the number of methylated genes and the methylation levels in individual genes between H pylori -positive and H pylori -negative sample results and between pediatric and adult samples.
  
  
  RESULTS
  The average number of methylated genes was significantly higher in H pylori -infected pediatric samples than in H pylori -negative pediatric samples (3.4 versus 0.3, P < .001) and in H pylori -infected adult samples than in H pylori -negative adult samples (7.6 versus 0.9, P < .001). Seven genes showed significantly higher methylation levels in H pylori -infected pediatric samples than in H pylori -negative pediatric samples (all values were P < .05).
  
  
  CONCLUSIONS
  These results indicate that CpG island hypermethylation occurs in pediatric gastric mucosa in association with H pylori infection and that the genes affected by H pylori -associated hypermethylation were similar in pediatric and adult samples.
authors.affiliation: Laboratory of Epigenetics, Cancer Research Institute, Seoul National University College of Medicine, Korea.
authors.forename: So-Hyun
authors.initials: SH
authors.lastname: Shin
authors.forename: Seog-Yun
authors.initials: SY
authors.lastname: Park
authors.forename: Jae-Sung
authors.initials: JS
authors.lastname: Ko
authors.forename: Nayoung
authors.initials: N
authors.lastname: Kim
authors.forename: Gyeong Hoon
authors.initials: GH
authors.lastname: Kang
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015703:Antigens, CD; D001706:Biopsy; D015820:Cadherins / Q000235:genetics; D002648:Child; D002675:Child, Preschool; D018899:CpG Islands / Q000235:genetics*; D019175:DNA Methylation / Q000235:genetics*; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism / Q000473:pathology*; D020868:Gene Silencing; D016481:Helicobacter Infections / Q000235:genetics* / Q000378:metabolism / Q000473:pathology*; D016480:Helicobacter pylori / Q000276:immunology / Q000302:isolation & purification; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000473:pathology; D017422:Sequence Analysis, DNA; D019717:Tissue Inhibitor of Metalloproteinase-3 / Q000235:genetics
chemical_list: D015703:Antigens, CD; C513384:CDH1 protein, human; D015820:Cadherins; C088390:TIMP3 protein, human; D019717:Tissue Inhibitor of Metalloproteinase-3