ReviewCell communication and signaling : CCS2013
The functional interplay of Helicobacter pylori factors with gastric epithelial cells induces a multi-step process in pathogenesis.
Review in Cell communication and signaling : CCS, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
96 citing papers in PubMed, 2 syntheses or guidelines pooled it, 179 citations in OpenAlex.
- Infiltration to infection: key virulence players of Helicobacter pylori pathogenicity.Infection · 2024Pooled it
- CagA toxin and risk of Helicobacter pylori-infected gastric phenotype: A meta-analysis of observational studies.PloS one · 2024Pooled it
- Host andGut microbes · 2026Article
- Coexist or eliminate? Antibody-based functional silencing versus eradication in gut microbiome- targeted therapy.Frontiers in immunology · 2026Review
- Navigating the gastric frontier of mucosal immunity againstFrontiers in immunology · 2026Review
- Use of bidirectional Mendelian randomization to unveil the association of Helicobacter pylori infection and pancreatic cancer.Medicine · 2025Article
- A study of the association betweenOncology letters · 2025Article
- The immunoregulatory role of helper T cells inFrontiers in immunology · 2025Review
- The oral-gut axis in chronic atrophic gastritis: current perspectives and integrated strategies.Frontiers in immunology · 2025Review
- Article
- The immunopathogenesis ofFrontiers in microbiology · 2024Review
- Design of aFrontiers in immunology · 2024Article
- Ebselen: A Promising Repurposing Drug to Treat Infections Caused by Multidrug-Resistant Microorganisms.Interdisciplinary perspectives on infectious diseases · 2024Review
- Diminishing of Helicobacter pylori adhesion to Cavia porcellus gastric epithelial cells by BCG vaccine mycobacteria.Scientific reports · 2023Article
- Reactive Oxygen Species andAntioxidants (Basel, Switzerland) · 2023Review
- ABO, Lewis blood group systems and secretory status with H.pylori infection in yemeni dyspeptic patients: a cross- sectional study.BMC infectious diseases · 2023Article
- Trimer stability of Helicobacter pylori HtrA is regulated by a natural mutation in the protease domain.Medical microbiology and immunology · 2023Article
- Searching for serum biomarkers linking coronary heart disease and Helicobacter pylori infection using infrared spectroscopy and artificial neural networks.Scientific reports · 2022Article
- Host Cell Antimicrobial Responses againstInternational journal of molecular sciences · 2022Review
- Incorporating Immunotherapy in the Management of Gastric Cancer: Molecular and Clinical Implications.Cancers · 2022Review
36 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Infections with the human pathogen Helicobacter pylori (H. pylori) can lead to severe gastric diseases ranging from chronic gastritis and ulceration to neoplastic changes in the stomach. Development and progress of H. pylori-associated disorders are determined by multifarious bacterial factors. Many of them interact directly with host cells or require specific receptors, while others enter the host cytoplasm to derail cellular functions. Several adhesins (e.g. BabA, SabA, AlpA/B, or OipA) establish close contact with the gastric epithelium as an important first step in persistent colonization. Soluble H. pylori factors (e.g. urease, VacA, or HtrA) have been suggested to alter cell survival and intercellular adhesions. Via a type IV secretion system (T4SS), H. pylori also translocates the effector cytotoxin-associated gene A (CagA) and peptidoglycan directly into the host cytoplasm, where cancer- and inflammation-associated signal transduction pathways can be deregulated. Through these manifold possibilities of interaction with host cells, H. pylori interferes with the complex signal transduction networks in its host and mediates a multi-step pathogenesis.
Indexed as
Identifiers
What OpenQuestion holds
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.