Expression of NF-kappaB in Helicobacter pylori infection

Helicobacter pylori colonizes the gastric mucosa in humans and causes chronic gastritis. NF-kappaB has a key role as a mediator in mucosal inflammation. In this study, we examined the expression of NF-kappaB in the antral epithelial cells of H. pylori-infected and H. pylori-uninfected biopsies and e...

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Bibliographic Details
Published in:Digestive diseases and sciences 2006-12, Vol.51 (12), p.2306-2309
Main Authors: Doger, Furuzan Kacar, Meteoglu, Ibrahim, Ozkara, Esra, Erkul, Zehra Kocakaya, Okyay, Pinar, Yükselen, Vahit
Format: Article
Language:English
Subjects:
Atrophy - pathology
Biopsy
Epithelial Cells - metabolism
Epithelial Cells - microbiology
Epithelial Cells - pathology
Gastric Mucosa - metabolism
Gastric Mucosa - microbiology
Gastric Mucosa - pathology
Gastritis - metabolism
Gastritis - microbiology
Gastritis - pathology
Gene Expression Regulation, Bacterial
Helicobacter Infections - genetics
Helicobacter Infections - metabolism
Helicobacter Infections - pathology
Helicobacter pylori
Humans
Metaplasia - pathology
NF-kappa B - genetics
NF-kappa B - metabolism
Retrospective Studies
Severity of Illness Index
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Summary:Helicobacter pylori colonizes the gastric mucosa in humans and causes chronic gastritis. NF-kappaB has a key role as a mediator in mucosal inflammation. In this study, we examined the expression of NF-kappaB in the antral epithelial cells of H. pylori-infected and H. pylori-uninfected biopsies and examined these processes in relationship with grade and activity of gastritis, density of H. pylori, presence of the intestinal metaplasia, and atrophy. Fifty biopsies (35 H. pylori-positive patients and 15 H. pylori-negative controls) were studied. NF-kappaB immunohistochemical stain was performed. NF-kappaB activity in H. pylori-infected biopsies were markedly enhanced compared with uninflamed biopsies (P = 0.001). We also found positive correlation NF-kappaB expression with severity of gastritis (according to Sydney score) (P = 0.001), activity of gastritis (P = 0.046) and H. pylori load (P < 0.001), and atrophy (P = 0.004). We did not find a significant relationship between NF-kappaB and the presence of intestinal metaplasia (P = 0.355). These findings suggested that expression of NF-kappaB has an important role in H. pylori gastritis.
ISSN:0163-2116