Gastric mucin

Gastric epithelium is protected by a mucus layer rich in MUC5AC and MUC6 mucins synthesised by the superficial epithelium and the glands, respectively. These cell populations also express specific fucosyltransferases that determine the glycosylation pattern of these gastric mucins. The maintenance of the structure and properties of the gastric mucus has been related to the degree of glycosylation and the oligomeric forms of the mucins. In gastric tumors, and in early preneoplastic lesions such as intestinal metaplasia, the glycosylation pattern detected in normal stomach is lost and, intestinal mucins, MUC2 and MUC4, can be ectopically detected in the gastric epithelium. These changes are biologically relevant because the binding of Helicobacter pylori to the gastric mucosa is mediated by blood group-related antigens. In vitro and animal models allowing the study of the gastric ecological niche and the requirements for its maintenance are essential for an understanding of the role of bacterial-mucosal interactions in pathological processes such as inflammation and cancer.

Background:Patients infected by Helicobacter pylori who have first-degree relatives with gastric cancer have an 8-fold increased risk of developing gastric cancer themselves. Mucins are high-molecular-weight glycoproteins that play a cardinal role in the protective mechanism of the gastric epithelium.Aim:To study gastric acid and mucin secretion in dyspeptic patients with and without a family history of gastric cancer and H. pylori infection.Materials and methods:Twenty-six dyspeptic patients underwent esophago-gastro-duodenoscopy, gastric biopsies, and acid and mucin secretory tests. The sample was divided by family history of gastric cancer and H. pylori status.Results:Patients who were infected by H. pylori had a significantly higher degree of inflammation than those who were not. H. pylori-positive patients with a positive family history had a lower basal and maximal gastric acid output than infected patients with no family history and noninfected controls, and a higher basal and maximal mucin output than infected patients with no family history. MUC5AC was the major mucin species expressed in gastric juice.Conclusions:In patients with relatives with gastric cancer, H. pylori infection is associated with a more severe inflammatory reaction consisting of decreased gastric acid secretion and increased mucin secretion.

Aim:To investigate the relationship between Helicobacter pylori (H. pylori) and mucin expression in gastric mucosa.Methods:English Medical literature searches were conducted for gastric mucin expression in H. pylori infected people vs uninfected people. Searches were performed up to December 31(th) 2014, using MEDLINE, PubMed, EMBASE, Scopus, and CENTRAL. Studies comparing mucin expression in the gastric mucosa in patients positive and negative for H. pylori infection, were included. Meta-analysis was performed by using Comprehensive meta-analysis software (Version 3, Biostat Inc., Englewood, NJ, United States). Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated compared mucin expression in individual studies by using the random effects model. Heterogeneity between studies was evaluated using the Cochran Q-test, and it was considered to be present if the Q-test P value was less than 0.10. I(2) statistic was used to measure the proportion of inconsistency in individual studies, with I(2) > 50% representing substantial heterogeneity. We also calculated a potential publication bias.Results:Eleven studies, which represent 53 sub-studies of 15 different kinds of mucin expression, were selected according to the inclusion criteria. Every kind of mucin has been considered as one study. When a specific mucin has been studied in more than one paper, we combined the results in a nested meta-analysis of this particular mucin: MUC2, MUC6, STn, Paradoxical con A, Tn, T, Type 1 chain mucin, LeA, SLeA, LeB, AB-PAS, MUC1, and MUC5AC. The odds ratio of mucin expression in random analysis was 2.33, 95%CI: 1.230-4.411, P = 0.009, higher expression in H. pylori infected patients. Odds ratio for mucin expression in H. pylori positive patients was higher for MUC6 (9.244, 95%CI: 1.567-54.515, P = 0.014), and significantly lower for MUC5AC (0.447, 95%CI: 0.211-0.949, P = 0.036). Thus, H. pylori infection may increase MUC6 expression and decrease MUC5AC expression by 924% and 52%, respectively.Conclusion:H. pylori inhibits MUC5AC expression in the gastric epithelium, and facilitates colonization. In contrast, increased MUC6 expression may help inhibiting colonization, using MUC6 antibiotics properties.