Role of mucin Lewis status in resistance to Helicobacter pylori infection in pediatric patients.

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