Glycosylation of mucins present in gastric juice: the effect of helicobacter pylori eradication treatment

Abstract

It is suggested that gastric mucins, and in particular some specific glycan structures that can act as carbohydrate receptors, are involved in the interactions with Helicobacter pylori adhesins. The main aim of our study was to evaluate glycosylation pattern of glycoproteins of gastric juice before and at the end of eradication therapy. Gastric juices were taken from 13 clinical patients and subjected to analysis. Pooled fractions of the void volume obtained after gel filtration were subjected to ELISA tests. To assess the relative amounts of carbohydrate structures, lectins and monoclonal antibodies were used. Changes in the level of MUC 1 and MUC 5AC mucins and of carbohydrate structures, which are suggested to be receptors for Helicobacter pylori adhesins, were observed by the end of the eradication treatment. Our results support the idea about the involvement of MUC 5AC and MUC 1 with some specific sugar structures in the mechanism of Helicobacter pylori infection.

Helicobacter pylori Containing More Phosphorylation Sites of the CagA Protein Induces Greater Reduction of Gastric Mucins

“…Similar results were obtained infection, but the reduction of the MUC5AC and MUC1 expression was more intense. The findings about the reduction of mucins associated with H. pylori infection are supported by the work of other authors [4,14,17,19]. Navabi et al [19] showed a reduction in the MUC1 production and a decreasing trend in the production of MUC5AC of the gastric antrum of mice infected with H. pylori [19].…”

“…Several authors have demonstrated that infection by H. pylori interferes with the gastric mucin content [15,17,19]. However, this is the first study to demonstrate reduction in the gastric mucin expression of gerbils infected with CagA positive H. pylori strains containing one or three phosphorylation sites using an accurate morphometric digital method.…”

“…When H. pylori was still known as Campylobacter pyloridis, it was found that infection with this bacterium is able to interfere with t mucus layer, leading to its reduction [20]. However, the mechanisms involved in these alterations are not fully understood and there is Several authors have demonstrated that infection interferes with the gastric mucin content [15,17,19]. However, this is the first study to demonstrate reduction in the gastric mucin expression of gerbils infected with CagA positive strains containing one or three EPIYA C phosphorylation sites using an accurate Campylobacter it was found that infection with this bacterium is able to interfere with the gastric mucus layer, leading to its reduction [20].…”

“…H. pylori seems to interfere in the MUC1 and MUC5AC glycosylation process, favoring the interaction of bacterial adhesins with the gastric epithelial surface and contributing with the bacteria colonization [17]. Furthermore, H. pylori releases urease, which degrades urea and releases ammonia, raising the gastric pH.…”

“…Some papers relate mucin content with H. pylori infection, both in humans and experimental models [15][16][17]. However, there is no study relating the content of specific mucins to infection by strains of CagA positive H. pylori with more than one phosphorylation site.…”