Role of Mucin Lewis Status in Resistance to Helicobacter pylori Infection in Pediatric Patients

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. 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.

Aeromonas salmonicida Growth in Response to Atlantic Salmon Mucins Differs between Epithelial Sites, Is Governed by Sialylated and N -Acetylhexosamine-Containing O -Glycans, and Is Affected by Ca 2+

“…The presence of GlcNAc may signal to the pathogen that it is in the mucus niche, and downregulating such factors may in turn free up more resources for growth. Indeed, in the human stomach, evidence suggests that downregulating pathogen binding to the gastric mucins is beneficial for the pathogen, as its removal from the gastric niche is decreased (43), and the pathogen decreases the level of adhesins after culture with mucins carrying the ligand to which it adheres (44).…”

Helicobacter pylori—Associated Dyspepsia in Paediatrics

“…Recently, it was shown that H. pylori-infected children presented a normal pattern of expression and glycosylation of mucin 5AC (MUC5AC) in the surface mucous cells, and MUC6 in the gland mucous cells, contrasting with the aberrant expression of MUC6 and MUC2 found in infected adults. Additionally, it was shown that the pattern of Lewis blood group antigens in the surface epithelium of children was significantly correlated with H. pylori load, however no correlation with gastritis, nodularity, and gastric or duodenal ulcer was found [17].…”

“…Nevertheless, H. pylori-associated peptic ulcer disease may also occur shortly after infection in childhood [4][5][6][7][8]. This rare event may be due to more virulent strains [9][10][11][12][13][14][15][16], and/or more predisposed subjects [17][18][19]. The two forms of H. pylori-associated peptic ulcers, i.e., gastric ulcer and duodenal ulcers, are divergent in prevalence and physiopathology, but both cause considerable patients' morbidity entailing high annual costs of treatment [93].…”

“…If often asymptomatic, the H. pylori-associated non-ulcer dyspepsia is clearly the strongest aetiological factor for severe gastric diseases that will develop late in adult life in a minority of infected patients, i.e., peptic ulcer disease, both gastric and duodenal ulcers, and gastric cancer, namely, adenocarcinoma and mucosa associated lymphoid tissue (MALT) lymphoma (reviewed in [3]). Peptic ulcer disease rarely occurs soon after H. pylori infection [4][5][6][7][8] that generally starts in childhood; this presumably reflects marked differences in the virulence [9][10][11][12][13][14][15][16] and/or in the susceptibility of young patients [17][18][19].…”

Common Genetic Variations in the MUC5AC Gene are Not Related to Helicobacter pylori Serologic Status

“…Normal gastric mucosa shows cell type specific expression of secreted mucin MUC5AC in the surface epithelium (Wang et al, 2006;Lindén et al, 2010). Several studies have strongly suggested that MUC5AC forms the major receptor for H. pylori in the human stomach (Van de Bovenkamp et al, 2003;Lindén et al, 2008), and the infection of H. pylori can alter the expression of MUC5AC (Kocer et al, 2004).…”