Background & Aims: Helicobacter pylori attaches to mucin oligosaccharides that are expressed on host gastric epithelium. We used the rhesus macaque model to characterize the effect of H pylori infection on gastric mucin oligosaccharides during acute and chronic infection. Methods: Specific pathogen (H pylori)-free rhesus macaques were inoculated with H pylori J166. Biopsy specimens of the gastric antrum were obtained 2 and 4 weeks before and 2, 8, and 24 weeks after infection with H pylori. O-linked mucin oligosaccharides were released from gastric biopsy samples by β-elimination and profiled by matrix-assisted laser desorption/ionization mass spectrometry. Similar studies were performed on gastric biopsy samples from H pylori-infected and uninfected humans. Formalin-fixed, paraffin-embedded sections of rhesus antrum biopsy samples were stained with H&E, periodic acid-Schiff stain, and antibody to MUC5AC, the predominant mucin expressed in the stomach. Results: H pylori-induced gastritis was accompanied by an acute and dramatic decrease in diversity and relative abundance of O-linked mucin oligosaccharides in the rhesus stomach, which largely recovered during the 24-week observation period. These variations in oligosaccharide abundance detected by mass spectrometry were reflected by changes in periodic acid-Schiff-positive material and expression of MUC5AC over time. Relatively few differences were seen in gastric mucin oligosaccharide composition between H pylori-infected and uninfected patients, which is consistent with the results in rhesus macaques because infection occurs in childhood. Conclusions: Acute H pylori infection is accompanied by a dramatic but transient loss in mucin oligosaccharides that may promote colonization and persistence.
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