Study on adhesion of Helicobacter pylori to stomach mucosa tissue
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Aim:To investigate the adhering ability and characteristics of Helicobacter pylori (HP) to gastric mucosa and the role of adhesion process in pathogenicity of HP.Methods: Ten HP strains were tested by adhering to stomach mucosa of 4 fetuses ageing from 6 to 8 months.Results: The average numbers of different HP strains adhering to fetal mucosa were very different.The numbers of HP on every tissue piece varied form 51 to 3 700. There were also significant differences in adhering numbers of HP strain in the same site of different fetus' stomaches and in different sites of one stomach. No matter how many germs which adhered to stomach,the gastric mucosa's pathological change of all corresponding patients exceeded middle degree.Conclusion: It is indicated that the number of HP adhered to stomach mucosa is influenced not only by the kinds and quantity of adhesion but also by the kinds and quantites of their corresponding receptors distributing on different gastric mucosa. Although adhesion of HP is a crucial progress in pathogenicity, the adhering ability of HP to stomach mucosa is not the only key factor.Cite
ABSTRACT Background and objectives. Helicobacter pylori shows a characteristic tropism for the mucus‐producing gastric epithelium. In infected patients, H. pylori colocalizes in situ with the gastric secretory mucin MUC5AC. The carbohydrate blood‐group antigen Lewis B (LeB) was deemed responsible for the adherence of H. pylori to the gastric surface epithelium. We sought to determine if MUC5AC is the carrier of LeB, and thus if MUC5AC is the underlying gene product functioning as the main receptor for H. pylori in the stomach. Methods. We studied three types of human tissue producing MUC5AC: Barrett's esophagus (BE), normal gastric tissue, and gastric metaplasia of the duodenum (GMD). Tissue sections were immuno‐fluorescently stained for MUC5AC or LeB, and subsequently incubated with one of three strains of Texas red‐labeled H. pylori , one of which was unable to bind to LeB. We determined the colocalization of MUC5AC or LeB with adherent H. pylori . Results. The binding patterns for the two LeB‐binding strains to all tissues were similar, whereas the strain unable to bind to LeB did not bind to any of the tissues. In normal gastric tissue, the LeB‐binding strains always bound to MUC5AC‐ and LeB‐positive epithelial cells. In four nonsecretor patients, colocalization of the LeB‐binding strains was found to MUC5AC‐positive gastric epithelial cells. In BE, the LeB‐binding H. pylori strains colocalized very specifically to MUC5AC‐positive cells. MUC5AC‐producing cells in GMD contained LeB. Yet, LeB‐binding H. pylori not only colocalized to MUC5AC or LeB present in GMD, but also bound to the LeB‐positive brush border of normal duodenal epithelium. Conclusions. Mucin MUC5AC is the most important carrier of the LeB carbohydrate structure in normal gastric tissue and forms the major receptor for H. pylori .
Colocalization
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AIM--To study the ultrastructural appearances of Helicobacter pylori in antral and duodenal biopsy specimens and its relation with the epithelial cells. METHODS--Endoscopically obtained antral and duodenal biopsy specimens were examined using transmission electron microscopy and freeze fracture analysis. RESULTS--Most bacteria looked curved, but in the duodenal bulb coccoid bacteria were relatively common. Bacteria were often found around intercellular junctions. freeze fracture examination indicated abnormalities of the tight junction complexes in patients with H pylori infection. In many biopsy specimens bacteria were seen closely attached to the epithelial cell membrane by different forms of adhesion. In addition to what looked like intracytoplasmic penetration by bacteria, several examples of genuine penetration were observed. CONCLUSION--H pylori is commonly found adhering to epithelial cells. Occasionally, H pylori may also penetrate cells. These features may contribute to the pathogenic action of the organism.
Duodenal bulb
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In the presented study, an evaluation of influence of different Helicobacter species and gastritis on intensity of cellular proliferation in pyloric glands of pigs’ stomach was performed. Samples of gastric antral mucosa obtained from 38 slaughtered pigs with known Helicobacter sp. and gastric inflammation statuses were stained with haematoxylin-eosin and immunohistochemically, for Ki67 antigen expression. Proliferative activity of epithelial cells was assessed by determination of: a ratio of proliferative zone length to gastric crypts length, an average percentage of cells showing Ki67 expression in proliferative zones of antral glands, and value of mitotic index in glands’ proliferative zones. None of the comparisons revealed statistically significant differences between animal groups with or without gastric inflammation, as well as between groups with or without Helicobacter colonisation. Additionally, no statistically significant differences were found between the group of animals that were infected with Candidatus Helicobacter suis, and that with the stomach colonised by different species of Helicobacter microorganisms.
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Objective In order to understand the ability and characterization of adhesion of H.pylori and discuss the adhesion mechanism of H.pylori to stomach mucosa.Methods 10 H.pylori strains were tested to adhere to stomach mucosa of 4 fetus.Results It showed that there were different ability and characterization among strains to adhere stomach mucosa.Conclusions It was indicated that H.pylori could secret many kinds of adhesion and the kinds and qantities of their corresponding receptors distributing on different gastric mucosa were variable.It suggested that the process of adhesion of H.pylori was very complicated.
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Background. Helicobacter pylori has generally been observed only in the gastric mucous layer or in the spaces between gastric mucus ‐s ecreting cells and not in the gastric epithelial cells or in the lamina propria. The purpose of this study is to determine whether H. pylori invades the gastric mucosa, using an immunoelectron microscopical examination of human gastric mucosa infected with H. pylori. Materials and Methods. Five hundred gastric antral biopsy specimens were fixed in a periodate‐lysin‐paraformaldehyde solution, embedded in Lowicryl, sectioned, and examined with a light microscope. One hundred specimens moderately or severely infected with H. pylori were selected and were incubated with polyclonal rabbit anti– H. pylori antibody. The specimens were washed, incubated with 20 nm of colloidal gold–conjugated goat anti–rabbit IgG, stained with uranyl acetate and lead citrate, and observed with a transmission electron microscope. Results. In one case, a bacterium was observed within the cytoplasm of a gastric mucus ‐s ecreting cell; in another case, a few bacteria were observed within the cytoplasm of a stromal cell in the lamina propria. The bacteria could be differentiated from degenerated intracellular organelles by gold particles attached to the bacteria. Conclusion. H. pylori rarely invade the lamina propria and gastric cells.
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The spatial relations between bacteria and the affected tissues can indicate pathogenic mechanisms. This study was undertaken to define the spatial relation of Helicobacter pylori to the human gastric mucosa. Antibodies against gastric mucus and ruthenium red were used to stabilise the glycoprotein structure of the mucus and glycocalyces in antral biopsy specimens from eight patients infected with H pylori. The location of organisms and ultrastructural features were assessed using systematic scanning and transmission electron microscopy: 92 (2)% (mean (SE] of H pylori were in the pit mucus, and 7 (3)% were in the surface mucus; 60 (12)% of H pylori were close to epithelial cells, with only 5 (2)% located near the epithelial intercellular junctions. Fine filamentous strands extended between organisms and nearby epithelial cells, with few organisms in membrane to membrane contact. H pylori were not observed between, beneath, or within cells of the gastric mucosa. The preferred location of H pylori in the gastric antrum is within the pit mucus close to the epithelial cell surface, with no evidence that they have a direct toxic effect on the mucosa.
Chronic gastritis
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Pyloric Antrum
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Gastric chief cell
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Digestion
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Component (thermodynamics)
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Helicobacter Infections
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L David, A Teixeira, C Reis, A Peixoto, F Carvalho, F Santos Silva, M Sobrinho-Simões Institute of Molecular Pathology and Immunology of the University of Porto – IPATIMUP, Rua Dr. Roberto Frias, 4200 Porto, Portugal. Correspondence to: L David. (+351) 22 5570 799. E-mail: [email protected] *This paper was an invited presentation at the 18 th Annual Symposium of European Cancer Prevention Organisation (ECP): Precancerous lesions of the digestive tract held in Maastricht, The Netherlands, 12–14 October, 2000 Mucins are glycoproteins of the mucous gel that protects mucosas from environmental aggressions. The core protein backbone of mucins is heavily O -glycosylated in the numerous serine or threonine residues. Activation of genes coding for the apomucin and for individual glycosyltransferases, with unique donor–substrate specificity, are responsible for the large diversity of the final end-product. Inter-individual diversity of mucins is determined by the polymorphic nature of mucin genes and by the ABO histo-blood group and secretor genes. Further intra-individual tissue-specific diversity is dependent upon the activation of different mucin and glycosyltransferase genes. Our group has recently explored two different approaches to the potential relationship between mucin constitution/expression and the outcome of Helicobacter pylori infection: a. The relationship between constitutional MUC1 mucin gene polymorphism and different lesions in the gastric carcinogenesis pathway. Our data show that individuals with a small number of tandem repeats, with smaller glycoprotein products, have an increased risk for the development of chronic atrophic gastritis, incomplete intestinal metaplasia and gastric carcinoma (Carvalho F (1997) Glycoconj J14: 107; Garcia E (1997) Cancer Epidemiol Biomarkers Prev6: 1071). b. The relationship between the pattern of mucin expression and H. pylori colonization of intestinal metaplasia. Our results show that H. pylori colonizes rare cases of incomplete intestinal metaplasia that do not express the intestinal mucin MUC2, thus suggesting that absence of MUC2 is a prerequisite for H. pylori adhesion to metaplastic mucosa (Reis CA (1999) Cancer Res59: 1003).
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