Aberrant CpG Island Hypermethylation in Pediatric Gastric Mucosa in Association With Helicobacter pylori Infection

Abstract

Context.—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. Objectives.—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. Design.—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.

The emerging role of epigenetics in the immune response to vaccination and infection: a systematic review

“…6 not 7 exp neoplasms/ or plant*1. • Mycobacterium tuberculosis [6,83,86,97,98] • Burkholderia pseudomallei [7] • Escherichia coli [104] • Anaplasma phagocytophilum [82] • Listeria monocytogenes [8,9,85] • Chlamydia trachomatis [90] • Porphyromonas gingivalis [87,89] • Fusobacterium nucleatum [89] • Bifidobacterium breve [10] • Lactobacillus rhamnosus GG [10] • Acinetobacter baumanni [11] • Pseudomonas aeruginosa [11] • Mycobacterium tuberculosis [12,[96][97][98] • Helicobacter pylori [13,14] • Gut microbiota (Bacteroides, Proteobacteria, Firmicutes) [111] • Placental microbiota [101] • Bacillus Calmette-Guérin [43] • Vaccinia Ankara MVA85A [47] • Bacillus Calmette-Guérin [15,44,45]…”

“…Nasal epith cells [27,113] [ 27] [27,113] HGEC [87] [ [87][88][89] TERT cells [89] NOK-SI cells Gastric mucosa [13] [ 13,14] Colonic mucosa [72] Huh7.5 cells HT-29/B6|T84 cells # [10] Bronch epith cells [11] U937 cells [7] A549 cells [25] [ [21][22][23][24] [ 22]…”