The Disease Spectrum of Helicobacter Pylori: The Immunopathogenesis of Gastroduodenal Ulcer and Gastric Cancer
Abstract
▪ Abstract Helicobacter pylori is a gram-negative bacterium that resides under microaerobic conditions in a neutral microenvironment between the mucus and the superficial epithelium of the stomach. From this site, it stimulates cytokine production by epithelial cells that recruit and activate immune and inflammatory cells in the underlying lamina propria, causing chronic, active gastritis. Although epidemiological evidence shows that infection generally occurs in children, the inflammatory changes progress throughout life. H. pylori has also been recognized as a pathogen that causes gastroduodenal ulcers and gastric cancer. These more severe manifestations of the infection usually occur later in life and in a minority of infected subjects. To intervene and protect those who might be at greatest risk of the more severe disease outcomes, it is of great interest to determine whether bacterial, host, or environmental factors can be used to predict these events. To date, several epidemiological studies have attempted to define the factors affecting the transmission of H. pylori and the expression of gastroduodenal disease caused by this infection. Many other laboratories have focused on identifying bacterial factors that explain the variable expression of clinical disease associated with this infection. An alternative hypothesis is that microorganisms that cause lifelong infections can ill afford to express virulence factors that directly cause disease, because the risk of losing the host is too great. Rather, we propose that gastroduodenal disease associated with H. pylori infection is predominantly a result of inappropriately regulated gastric immune responses to the infection. In this model, the interactions between the immune/inflammatory response, gastric physiology, and host repair mechanisms would dictate the disease outcome in response to infection.
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Chronic Helicobacter pylori infection is the world's leading cause of stomach cancer.
“whereas chronic Helicobacter pylori infection is the world’s leading cause of stomach cancer32.”
From Inflammation and cancer (2002) · cites this paper as [32]
H. pylori is established as a definite carcinogen for the development of gastric cancer, the second most common type of cancer globally, and DNA damage resulting from chronic inflammation is believed the mechanism.
“The Gram-negative bacterium H. pylori is established as a definite carcinogen for the development of gastric cancer — the second most common type of cancer globally11,29 — and DNA damage resulting from chronic inflammation is believed the mechanism32.”
From Inflammation and cancer (2002) · cites this paper as [32]
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- Authors
- Ernst, P. B., & Gold, B. D.
- Affiliations
- The University of Texas Medical Branch at Galveston (US)
- Centers for Disease Control and Prevention (US)
- ORCID
- Ernst, Peter B.
- Venue
- Annual Review of Microbiology
- Publisher
- Annual Reviews
- Published
- 2000-10
- Volume
- 54
- Issue
- 1
- Pages
- 615-640
- ISSN
- 0066-4227 (ISSN-L)
- 1545-3251
- OpenAlex
- W2124635565
- Cited by
- 554
- References
- 135
- Citations by year
- 2026: 9 · 2025: 12 · 2024: 14 · 2023: 13 · 2022: 18 · 2021: 10 · 2020: 21 · 2019: 17 · 2018: 15 · 2017: 17 · 2016: 26 · 2015: 23 · 2014: 28 · 2013: 26 · 2012: 19
- FWCI
- 3.18
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annual Review of Microbiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK053708, DK-53708, R01DK050669, DK 51577, DK 50669)
- Topics
- Health Sciences › Medicine › Surgery › Helicobacter pylori-related gastroenterology studies
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
- Keywords
- Helicobacter pylori, immunopathogenesis, peptic ulcer, gastric cancer, chronic gastritis, inflammation, virulence factors, disease spectrum, risk factors, gastric physiology
- MeSH terms
- Adenocarcinoma, Duodenal Ulcer, Humans, Lymphoma, Stomach Neoplasms, Stomach Ulcer, Helicobacter pylori, Helicobacter Infections, Models, Immunological
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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