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      Pathogenesis of Helicobacter pylori infection.

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          Abstract

          Helicobacter pylori is the first formally recognized bacterial carcinogen and is one of the most successful human pathogens, as over half of the world's population is colonized with this gram-negative bacterium. Unless treated, colonization usually persists lifelong. H. pylori infection represents a key factor in the etiology of various gastrointestinal diseases, ranging from chronic active gastritis without clinical symptoms to peptic ulceration, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue lymphoma. Disease outcome is the result of the complex interplay between the host and the bacterium. Host immune gene polymorphisms and gastric acid secretion largely determine the bacterium's ability to colonize a specific gastric niche. Bacterial virulence factors such as the cytotoxin-associated gene pathogenicity island-encoded protein CagA and the vacuolating cytotoxin VacA aid in this colonization of the gastric mucosa and subsequently seem to modulate the host's immune system. This review focuses on the microbiological, clinical, immunological, and biochemical aspects of the pathogenesis of H. pylori.

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          Author and article information

          Journal
          Clin Microbiol Rev
          Clinical microbiology reviews
          American Society for Microbiology
          0893-8512
          0893-8512
          Jul 2006
          : 19
          : 3
          Affiliations
          [1 ] Department of Gastroenterology and Hepatology, Erasmus MC-University Medical Center, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands. j.g.kusters@erasmusmc.nl
          Article
          19/3/449
          10.1128/CMR.00054-05
          1539101
          16847081
          de821f1e-02e3-42a2-bb85-293f6f34bde1
          History

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