ArticleScientific reports2015
Mutual reinforcement of inflammation and carcinogenesis by the Helicobacter pylori CagA oncoprotein.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 60 citations in OpenAlex.
- Association Between Helicobacter pylori Exposure and Decreased Odds of Eosinophilic Esophagitis-A Systematic Review and Meta-analysis.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2019Pooled it
- Systematic review with meta-analysis: association between Helicobacter pylori CagA seropositivity and odds of inflammatory bowel disease.Alimentary pharmacology & therapeutics · 2019Pooled it
- Review
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- Exploratory metabolomic analysis for identifying systemic signatures ofFrontiers in immunology · 2026Article
- The oral-gastric microbial axis in children: salivary signatures as non-invasive biomarkers for pediatric gastritis andFrontiers in cellular and infection microbiology · 2026Review
- CagA-dependent expression of anti-inflammatory cytokine IL-13 and TNFRSF member Fn14 inFrontiers in microbiology · 2026Article
- Cancer microbiota: a focus on tumor-resident bacteria.EMBO reports · 2025Review
- Clinical characteristics of ulcerative colitis patients with different types ofMicrobiology spectrum · 2024Article
- Causality of Helicobacter pylori infection on eosinophilic esophagitis and potential pathogenesis: a Mendelian randomization study.Frontiers in immunology · 2024Article
- Bacteria in cancer initiation, promotion and progression.Nature reviews. Cancer · 2023Review
- Updated Epidemiology of Gastric Cancer in Asia: Decreased Incidence but Still a Big Challenge.Cancers · 2023Review
- Equilibria of complexes in the aqueous cobalt(II)-Computational and structural biotechnology journal · 2023Article
- Potential Antigenic Candidates for the Development of Peptide-Based Vaccines to Induce Immunization againstInternational journal of molecular sciences · 2022Article
- Antibodies towards TVLLPVIFF Amino Acid Sequence of TNF Receptor Induced byJournal of clinical medicine · 2022Article
- Exosomal CagA from Helicobacter pylori aggravates intestinal epithelium barrier dysfunction in chronic colitis by facilitating Claudin-2 expression.Gut pathogens · 2022Article
- Peripheral Cytokine Levels as a Prognostic Indicator in Gastric Cancer: A Review of Existing Literature.Biomedicines · 2021Review
- Chemical Characterization and Biological Evaluation of New Cobalt(II) Complexes with Bioactive Ligands, 2-Picolinehydroxamic Acid and Reduced Schiff BasePharmaceuticals (Basel, Switzerland) · 2021Article
- Interference of LPSCells · 2021Article
- EPIYA motifs ofNew microbes and new infections · 2021Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori cagA-positive strain delivers the CagA oncoprotein into gastric epithelial cells and at the same time elicits stomach inflammation. To experimentally investigate the pathophysiological interplay between CagA and inflammation, transgenic mice systemically expressing the bacterial cagA gene were treated with a colitis inducer, dextran sulfate sodium (DSS). Compared with control mice, DSS-induced colitis was markedly deteriorated in cagA-transgenic mice. In the colonic epithelia of cagA-transgenic mice, there was a substantial decrease in the level of IκB, which binds and sequesters NF-κB in the cytoplasm. This IκB reduction was due to CagA-mediated inhibition of PAR1, which may stimulate IκB degradation by perturbing microtubule stability. Whereas the CagA-mediated IκB reduction did not automatically activate NF-κB, it lowered the threshold of NF-κB activation by inflammogenic insults, thereby contributing to colitis exacerbation in cagA-transgenic mice. CagA also activates inflammasomes independently of NF-κB signaling, which further potentiates inflammation. The incidence of colonic dysplasia was elevated in DSS-treated cagA-transgenic mice due to a robust increase in the number of pre-cancerous flat-type dysplasias. Thus, CagA deteriorated inflammation, whereas inflammation strengthened the oncogenic potential of CagA. This work revealed that H. pylori CagA and inflammation reinforce each other in creating a downward spiral that instigates neoplastic transformation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.