Abstract
Helicobacter pylori (H. pylori) is a primary etiologic factor in gastric diseases. Sulglycotide is a glycopeptide derived from pig duodenal mucin. Esterification of its carbohydrate chains with sulfate groups creates a potent gastroprotective agent used to treat various gastric diseases. We investigated the inhibitory effects of sulglycotide on adhesion and inflammation after H. pylori infection in human gastric adenocarcinoma cells (AGS cells). H. pylori reference strain 60190 (ATCC 49503) was cultured on Brucella agar supplemented with 10% bovine serum. Sulgylcotide-mediated growth inhibition of H. pylori was evaluated using the broth dilution method. Inhibition of H. pylori adhesion to AGS cells by sulglycotide was assessed using a urease assay. Effects of sulglycotide on the translocation of virulence factors was measured using western blot to detect cytotoxin-associated protein A (CagA) and vacuolating cytotoxin A (VacA) proteins. Inhibition of IL-8 secretion was measured using enzyme-linked immunosorbent assay (ELISA) to determine the effects of sulglycotide on inflammation. Sulglycotide did not inhibit the growth of H. pylori, however, after six and 12 hours of infection on AGS cells, H. pylori adhesion was significantly inhibited by approximately 60% by various concentrations of sulglycotide. Sulglycotide decreased H. pylori virulence factor (CagA and VacA) translocation to AGS cells and inhibited IL-8 secretion. Sulglycotide inhibited H. pylori adhesion and inflammation after infection of AGS cells in vitro. These results support the use of sulglycotide to treat H. pylori infections.
Highlights
Helicobacter pylori (H. pylori) is a helical Gram-negative bacterium that penetrates gastric mucosa and colonizes the stomach [1]
We investigated the inhibitory effects of sulglycotide on adhesion and inflammation following H. pylori infection in human gastric adenocarcinoma cells (AGS cells)
Sulglycotide did not inhibit the growth of H. pylori at any of the tested concentrations, but growth varied depending on the concentration (Figure 1)
Summary
Helicobacter pylori (H. pylori) is a helical Gram-negative bacterium that penetrates gastric mucosa and colonizes the stomach [1]. H. pylori infection is associated with numerous gastric diseases [2,3], initiates acute inflammatory reactions and progresses chronic inflammatory reactions, atrophic gastric mucosal changes, intestinal metaplasia, dysplasia, and carcinogenesis, which is known as the inflammation-carcinoma chain [4]. H. pylori is classified as a type I carcinogen [1]. H. pylori infection might persist for many years without inducing gastrointestinal symptoms, even though 1% to. 3% of infected human hosts develop gastric cancer [5,6]. The prevalence of H. pylori infection exceeds half of the world’s population. In South Korea, the prevalence is 50% to 80% in 40–50-year-olds with approximately 12~49% of 16–19-year-olds infected [7], as such, gastric diseases including gastric cancer is likely to be high in South Korea
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