Hippokratia 2003, 7(4):173-176

K Charalabopoulos, V Papalimneou, NJ Agnantis

Abstract

Helicobacter pylori bacterium colonizes the gastric mucosa in humans causing chronic active gastritis type B and peptic ulcer disease. It is the commonest cause of antral gastric and duodenal ulceration. Furthermore, it is implicated in gastric adenocarcinoma, mucosal atrophy and low grade B-cell lymphoma of mucosa associated lymphoid tissue (MALT lymphoma). Re-infection of peptic ulcer is associated with re-infection by the bacterium.In contrast to other pathogens of the gastrointestinal tract, which invade the mucosal barrier, Helicobacter pylori, rarely penetrates the gastric epithelium. Typical histological pattern of inflammation is though observed in the submucosal layer. Antigens constantly found in all strains as well as some other found in certain strains of the bacterium, play an important role in the immune response of the human organism, apoptosis and signal transduction. Pathogenetic mechanisms involved in pathogenesis of various disease processes induced by helicobacter pylori are not yet fully elucidated. Adhesion molecules, interleukins and other inflammation mediators, participate in the hole process. In the present review article all these pathogenetic mechanisms are discussed in detail.

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