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Pathogenesis of Helicobacter pylori Infection
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SUMMARY: 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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“H. pylori infection can lead to antrum-predominant gastritis, in which the oxyntic mucosa is not inflamed but a gastrin-driven increase in acid output occurs, along with the possible development of duodenal ulcer[67,68].”
From Proton pump inhibitors and dysbiosis: current knowledge and aspects to be clarified (2019) · cites this paper as [67]
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Metadata
- Authors
- Kusters, J. G., van Vliet, A. H. M., & Kuipers, E. J.
- Affiliations
- Erasmus MC (NL)
- Department of Gastroenterology and Hepatology, Erasmus MC—University Medical Center, Rotterdam, The Netherlands
- Venue
- Clinical Microbiology Reviews
- Publisher
- American Society for Microbiology
- Published
- 2006-07
- Volume
- 19
- Issue
- 3
- Pages
- 449-490
- ISSN
- 0893-8512 (ISSN-L)
- 1098-6618
- PMC
- PMC1539101
- OpenAlex
- W2153354382
- Cited by
- 2,526
- References
- 732
- Citations by year
- 2026: 93 · 2025: 127 · 2024: 117 · 2023: 119 · 2022: 133 · 2021: 180 · 2020: 174 · 2019: 153 · 2018: 129 · 2017: 144 · 2016: 137 · 2015: 140 · 2014: 172 · 2013: 140 · 2012: 97
- FWCI
- 15.43
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Clinical Microbiology Reviews (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- RePub (Erasmus University Rotterdam) (submittedVersion, other-oa)
- Surrey Research Insight Open Access (The University of Surrey) (submittedVersion)
- Topics
- Health Sciences › Medicine › Gastroenterology › Helicobacter pylori-related gastroenterology studies
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Life Sciences › Agricultural and Biological Sciences › Food Science › Salmonella and Campylobacter epidemiology
- Keywords
- Helicobacter pylori, pathogenesis, bacterial colonization, chronic active gastritis, peptic ulcer, gastric adenocarcinoma, gastric MALT lymphoma, host-pathogen interaction, gastric acid secretion, CagA, VacA, virulence factors
- MeSH terms
- Animals, Gastritis, Guinea Pigs, Humans, Peptic Ulcer, Stomach Neoplasms, Helicobacter pylori, Helicobacter Infections, Virulence Factors, Mice
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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