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Helicobacter pylori Infection and the Pathogenesis of Duodenal Ulceration
Author(s) -
WALKER M. M.,
CRABTREE J. E.
Publication year - 1998
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1998.tb11114.x
Subject(s) - pathogenesis , helicobacter pylori , helicobacter infections , medicine , gastroenterology , duodenal ulcer , duodenal diseases , helicobacter , helicobacter pylori infection , duodenum , immunology
ABSTRACT:Helicobacter pylori is a gram‐negative spiral bacterium confined to the habitat of gastric‐type epithelium. H. pylori causes duodenal ulceration by a cumulative effect of antral predominant gastritis with increased acid secretion, consequent gastric metaplasia in the duodenum (a site of further colonization by H. pylori ), duodenitis, reduced duodenal bicarbonate secretion, and mucosal damage. Bacterial factors influence outcome. Major determinants are the production of a vacuolating toxin and the presence of CagA, an immunodominant product of a nonconserved gene cagA , a marker for the cag pathogenicity island that encodes virulence genes involved in induction of epithelial chemokine responses. In ulcer patients the mucosal immune response is polarized to a T‐helper‐1 (Th1) cell‐mediated response, which may contribute to mucosal damage. Eradication of H. pylori restores acid output to normal. Loss of both acid and bacteria halts gastroduodenitis and allows ulcer healing. Gastric metaplasia does not regress in the short term.