A confirmatory report for the close interaction of Helicobacter pylori with gastric epithelial MUC5AC expression

dc.authorid116537en_US
dc.contributor.authorKoçer, Havva Belma
dc.contributor.authorUlaş, Murat
dc.contributor.authorÜstündağ, Yücel
dc.contributor.authorErdoğan, Sibel
dc.contributor.authorKarabeyoğlu, Şerif Melih
dc.contributor.authorYıldırım, Osman
dc.contributor.authorÜnal, Bülent
dc.contributor.authorCengiz, Ömer
dc.date.accessioned2017-08-15T08:29:29Z
dc.date.available2017-08-15T08:29:29Z
dc.date.issued2004
dc.departmentİnönü Üniversitesien_US
dc.description.abstractHelicobacter pylori (H. pylori) infection is associated with the development of gastritis and peptic ulcer and is presumed to be a risk factor for low-grade B-cell lymphoma and gastric cancer. H. pylori also causes critical alterations in gastric mucin structure. Our aim was to determine the effect of H. pylori on MUC1, MUC2, and MUC5AC expression. METHODS: Thirty H. pylori-positive and 15 H. pylori-negative antral gastric endoscopic biopsy specimens were evaluated for MUC1, MUC2, and MUC5AC expression with immunohistochemical staining. From the same specimens, we scrutinized the presence of H. pylori infection by hematoxylin and eosin and immunohistochemical staining. RESULTS: In H. pylori infected patients, the expression of MUC5AC was found to be localized to the cells in the superficial epithelium and upper parts of the gastric glands. The number of MUC5AC-expressing cells and the staining intensity of MUC5AC were shown to decrease in patients with H. pylori infection. Histopathology and immunostaining patterns of gastric mucins implied that H. pylori was physically associated with extracellular MUC5AC and MUC5AC-producing cells. H. pylori infection does not significantly affect staining intensity and patterns of MUC1 and MUC2 expressions. MUC1 was not found in dysplastic tissues or intestinal metaplasia areas. MUC5AC was expressed in dysplastic areas, but not in intestinal metaplasia. MUC2 was expressed in both dysplastic and intestinal metaplasia areas. CONCLUSION: H. pylori decreases the amount of MUC5AC expression. With reducing MUC5AC-producing cells and MUC5AC mucin, H. pylori may potentially cause significant alterations of the structure and function of gastric mucins. H. pylori-dependent inhibition of mucin synthesis deserves more investigations to clarify the role of H. pylori and gastric MUC5AC interaction.en_US
dc.identifier.citationKoçer, H. B. Ulaş, M. Üstündağ, Y. Erdoğan, S. Karabeyoğlu, Ş. M. Yıldırım, O. Ünal, B. Cengiz, Ö. (2004). A confirmatory report for the close interaction of Helicobacter pylori with gastric epithelial MUC5AC expression. J Clin Gastroenterol. 38(6):496-502.en_US
dc.identifier.endpage502en_US
dc.identifier.issue6en_US
dc.identifier.startpage496en_US
dc.identifier.urihttps://hdl.handle.net/11616/7561
dc.identifier.volume38en_US
dc.language.isoenen_US
dc.publisherJ Clin Gastroenterol.en_US
dc.relation.ispartofJ Clin Gastroenterol.en_US
dc.rightsinfo:eu-repo/semantics/embargoedAccessen_US
dc.titleA confirmatory report for the close interaction of Helicobacter pylori with gastric epithelial MUC5AC expressionen_US
dc.typeArticleen_US

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