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To analyze the glycoprotein binding sites of the gastric mucosa and its secreted mucus using lectin histochemistry in patients with chronic non-atrophic gastritis (CNAG) associated or not-associated with Helicobacter pylori infection with or without dysplasia.In order to identify the areas with glycoconjugates expression in gastric mucosa, 6 lectins (Canavalia ensiformis agglutinin - Con A, Sambucus nigra agglutinin - SNA, wheat germ agglutinin - WGA, soybean agglutinin - SBA, Helix pomatia agglutinin - HPA, peanut agglutinin - PNA) were used. Carbohydrate determinants were visualized according to the lectin-peroxidase-diaminobenzidine staining protocol. Biopsy material was obtained and processed by conventional histological methods. The samples from 84 patients (54 with CNAG) with low (n = 34) and high grade (n = 20) dysplasia, 38 patients were H. pylori-infected and 26 patients - H. pylori-noninfected) were used. The comparison group included 30 persons with CNAG without dysplasia (16 patients H. pylori-infected and 14 - noninfected).In comparison to normal gastric mucosa, a low affinity of Con A was shown in 80% of patients with non-infected CNAG and 90% of H. pylori associated CNAG. In 70% of H. pylori-infected patients with CNAG and low grade dysplasia there was an increase of SNA expression compared with non-infected patients (p0.05). Regarding SBA labeling no differences were detected in the studied groups (p 0.05). In H. pylori infected patients with CNAG and low grade dysplasia, WGA, HPA and PNA showed a strong reactivity with the gastric mucosa cells in 80; 75%, and 60% of patients, respectively.We suggest that a set of lectins in reaction with gastric epithelial and glandular cells can be used as a tool to obtain information about the dysplastic changes of the gastric mucosa and may offer new insight into gastric carcinogenesis and precancerous lesions treatment.

To assess the profile of mucins (MUC1, MUC2, MUC5AC) in gastric mucosa through immunohistochemical method.To identify metaplastic areas in gastric mucosa there was used chromoendoscopy with 0.5% solution of methylene blue, the expression of the mucins profile was determined using immunohistochemistry with MUC1, MUC5AC, MUC2 and MUC6 antibodies (clone Ma695, clone CLH2, Ccp58 and CLH5, "Novocastra" Great Britain).In case of the complete intestinal metaplasia (IM) there was maximum MUC2 expression in goblet cells. MUC5AC, MUC1 and MUC6 expression were absent in columnar epitheliocytes with brush border. In case of incomplete IM along with positive MUC2 marking of goblet cells, in 25% of such patients with chronic atrophic gastritis with incomplete IM MUC5AC expression has been observed; but in columnar epitheliocytes MUC5AC expression was observed in 100% of patients, and MUC2 expression was detected in 15% of patients only. Weak expression of MUC2 and MUC5AC in the areas adjacent to gastric adenocarcinoma was registered.MUC5AC expression in columnar epithelial cells and goblet exocrinocytes marks the formation of gastrointestinal phenotype - incomplete IM, along with the simultaneous production of MUC2 by goblet cells. Decrease of MUC 5AC expression in columnar epithelial cells and goblet exocrinocytes was found in areas of severe dysplasia and IM that may serve as an additional criterion of early malignization of gastric mucosa cells.

Helicobacter pylori (H. pylori) is detected on the surface of gastric epithelium and in goblet cells, predominantly in patients with chronic atrophic gastritis and incomplete intestinal metaplasia (IM). H. pylori infection persistence leads to the formation of gastrointestinal phenotype of IM. H. pylori can be considered as an etiological factor of IM. It inhibits the expression of SOX2 in gastric epithelial cells, hence activating transcription factor CDX2 as a counterpart to MUC5AC gene inhibition and MUC2 gene induction. Thus, in metaplastic cells, programming differentiation after intestinal phenotype will develop. The role of H. pylori in the origin of intestinal metaplasia of gastric mucosa was defined in this study to elucidate the probable mechanism of cell reprogramming. The activation of CDX2, with simultaneous inactivation and decreased number of genes (e.g., SHH, SOX2, and RUNX3) responsible for gastric differentiation, was identified to cause the appearance of IM.