The epithelial changes associated with Helicobacter pylori infection: the biology of gastric and intestinal metaplasia
It is now abundantly clear that Helicobacter pylori has an aetiological role in the pathogenesis of chronic gastritis and peptic ulcer in both the stomach and the duodenum1,2, and highly likely that it is incriminated in the induction of carcinoma of the stomach3 and low-grade gastric (MALT) lymphoma4. However, the actual mechanisms by which this organism exerts its effects have not yet been elucidated. What is clear is that colonization and adhesion of the bacteria to the mucosal surface, followed either by the production of toxin(s) and/or mucosal invasion, are the prerequisites for induction of tissue damage. This implies that adhesion of the organism to the epithelial cells of the gastroduodenal mucosa is an extremely important step. The organism maintains a microenvironment with a more neutral pH immediately adjacent to the mucosa5, with direct adhesion of the organism to the apical plasma membrane of the epithelial cell to form the characteristic adhesion pedestal6, with some authors suggesting a preference for intercellular junctions7.
KeywordsDuodenal Ulcer Pylorus Infection Intestinal Metaplasia Clinical Cure Paneth Cell
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