Role of mucin Lewis status in resistance to Helicobacter pylori infection in pediatric patients - PubMed (original) (raw)
Role of mucin Lewis status in resistance to Helicobacter pylori infection in pediatric patients
Sara Lindén et al. Helicobacter. 2010 Aug.
Abstract
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.
Materials and 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 Le(b) and Le(a) blood group antigens were present in the surface epithelium of 80% and 29% of children, respectively. H. pylori load was higher in Le(b) negative children than in Le(b) positive individuals (mean +/- SEM 17.8 +/- 3.5 vs 10.8 +/- 1.5; p < 0.05), but there was no correlation between Le(a) or Le(b) status and gastritis, nodularity, and gastric or duodenal ulcer (DU). Expression of sialyl-Le(x) 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 Le(b) positive children indicates that H. pylori is suppressed in the presence of gastric mucins decorated with Le(b), the binding site of the H. pylori BabA adhesin.
Figures
Figure 1. H. pylori in antral gastric gland
H. pylori colonization in superficial gland of a child with duodenal ulcer in two 5-μm-thick serial sections (Original magnification X1000). (A) 1_6S rRNA_ in red (FISH-Texas red); (B) cagA in green (FISH-FITC); (C) merge of A and B, demonstrating colocalization of 16S rRNA and cagA (in yellow) in the same bacteria. Note that only cagA (green) is expressed in the outer part of bacteria while both 16S rRNA and cagA are co-localized in the center (yellow); (D) Genta stain of a gastric gland, showing many curved _H. pylori-_shaped bacteria colonizing the lumen mucus or adherent to the apical part of mucus-secreting cells. Note that some of the bacteria appear intensely stained black by silver, while others are weakly stained (in part or completely). These variations may represent different capture of silver stain and may be due to the presence of mucus on part of the bacterial membrane.
Figure 2. Tissue localization of mucins and carbohydrate antigens
Section from a H. pylori negative patient was stained brown using immunohistochemistry for MUC5AC (A). Sections from H. pylori positive patients were stained brown for MUC6 (B), Leb (C), Sialyl-Lex (D) and Sialyl-Lea (E).
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