Background Helicobacter pylori causes gastritis, peptic ulcer and is a risk factor for adenocarcinoma and lymphoma of the stomach. Gastric mucins, carrying highly diverse carbohydrate structures, present functional binding sites for H. pylori and may play a role in pathogenesis. However, little information is available regarding gastric mucin in children with and without stomach diseases. Material & Methods Expression of mucins and glycosylation was studied by immunohistochemistry on gastric biopsies from 51 children with and without H. pylori infection and/or peptic ulcer disease. Results In all children, MUC5AC was present in the surface epithelium and MUC6 in the glands. No MUC6 in the surface epithelium or MUC2 was detected in any section. The Leb and Lea blood-group antigens were present in the surface epithelium of 80% and 29% of children respectively. H. pylori load was higher in Leb negative children than in Leb positive individuals (means ± SEM 17.8±3.5 vs 10.8±1.5; p < 0.05), but there was no correlation between Lea or Leb status and gastritis, nodularity, and gastric or duodenal ulcer. Expression of sialyl-Lex was associated with H. pylori infection, and DU. Conclusions Mucin expression and glycosylation is similar in children and adults. However, in contrast to adults, pediatric H. pylori infection is not accompanied by aberrant expression of MUC6 or MUC2. Furthermore, the lower H. pylori density in Leb positive children indicates that H. pylori is suppressed in the presence of gastric mucins decorated with Leb, the binding site of the H. pylori BabA adhesin.

Gastroduodenal disease is more common among adults and children with cagA+ H. pylori infection, but disease severity varies among those infected with cagA+ strains. We examined whether cagA in situ expression can predict disease manifestations among H. pylori infected children. Fifty-one children were selected from 805 patients with abdominal symptoms who underwent esophagogastroduodenoscopy with gastric biopsies. Endoscopic and histologic gastritis were scored and H. pylori colonization was quantified by Genta stain and in situ hybridization expression of 16S rRNA and cagA. Endoscopy was either normal (n=14) or demonstrated nodularity (n=18), gastric ulcer (GU, n=8) or duodenal ulcer (DU, n=11). H. pylori was present in 7, 18, 6, and 10 children, respectively. Expression of 16S rRNA and cagA were significantly higher in children with ulcer compared to normal. The fraction of H. pylori bacteria expressing cagA in situ was higher in children with ulcer compared to those with endoscopic nodularity (p<0.05). Thus, cagA in situ expression is increased in H. pylori infected children with peptic ulcers and may play a role in the pathogenesis of peptic ulcer disease during childhood. Determination of in situ expression of cagA complements traditional isolation and in vitro testing of single colony isolates. • JR and MG designed and performed the study, analyzed the data and revised the manuscript; CSM mentored JR and MG, supervised performance and analysis of in situ hybridization studies, and revised the manuscript; HL designed and validated the probes used for in situ hybridization studies, and revised the manuscript; CO performed the statistical analysis and revised the manuscript; ERP reviewed and graded histopathology sections and revised the manuscript; CS helped in the analysis of the clinical data and revised the manuscript; and AD closely supervised and participated in the design and performance of all the steps of the study, and revised the manuscript.

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