ArticlePloS one2019
The effect of Helicobacter pylori infection and different H. pylori components on the proliferation and apoptosis of gastric epithelial cells and fibroblasts.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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
48 citing papers in PubMed, 81 citations in OpenAlex.
- Vascular plasticity in the gastric cancer environment: mechanisms, prognostic significance, and concepts of therapeutic interventions.Cancer metastasis reviews · 2026Review
- Differential apoptosis of GES-1 cells induced by Helicobacter pylori with heteroresistance to clarithromycin.Archives of microbiology · 2026Article
- Mechanistic Insights into the Action of Histamine-Functionalized PLA Nanoparticles Loaded with 5-Fluorouracil Against Gastric Cancer CellsMolecules (Basel, Switzerland) · 2026Article
- Beyond the Stomach: Exploring the Role ofExpert reviews in molecular medicine · 2026Review
- Epithelial cell-derived exosomes carry NamiRNA-143-5p and promote ASPN expression in fibroblasts to induce Helicobacter pylori infected gastritis progression.Gut pathogens · 2026Article
- Hydrogen Sulfide InhibitsCells · 2026Article
- New concepts of chitosan-based mucosal formulations for supporting control of the gastric pathogenFrontiers in microbiology · 2026Review
- Upregulation of innate and adaptive immune mechanisms facilitating prevention of gastricFrontiers in immunology · 2026Article
- Development of 3D spheroids of AGS gastric cancer cellsFrontiers in microbiology · 2026Article
- Review
- Complex forming properties of cannabinoid acids in a green solvent and bioassays focused on gastric disease caused by Helicobacter pylori infection.Scientific reports · 2025Article
- Doxorubicin loaded polylactide nanoparticles functionalized histamine promote apoptosis of human gastric cancer cells AGS.Scientific reports · 2025Article
- Untargeted metabolomic profiling for identifying systemic signatures of helicobacter pylori infection in a guinea pig model.Scientific reports · 2025Article
- Helicobacter pylori and gastric cancer: mechanisms and new perspectives.Journal of hematology & oncology · 2025Review
- A critical review onFrontiers in cellular and infection microbiology · 2025Review
- The Effect ofAdvanced biomedical research · 2025Article
- Kill Two Birds with One Stone? The Effect ofCancers · 2024Review
- Current Knowledge about Gastric Microbiota with Special Emphasis onCurrent issues in molecular biology · 2024Review
- Helicobacter pylori components increase the severity of metabolic syndrome and its hepatic manifestations induced by a high fat diet.Scientific reports · 2024Article
- Spray-dried pH-sensitive chitosan microparticles loaded with Mycobacterium bovis BCG intended for supporting treatment of Helicobacter pylori infection.Scientific reports · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHelicobacter pylori colonizes the human gastric mucosa, causing chronic inflammation, peptic ulcers and gastric cancer. A cascade of harmful processes results from the interaction of these bacteria with the gastric epithelium.
aimTo investigate these processes in terms of upregulation of oxidative stress and cell apoptosis and downregulation of the pro-regenerative activity of cells.
methodsWe employed an in vivo guinea pig model at 7 or 28 days postinoculation with H. pylori, corresponding to an acute or chronic stage of infection, respectively, and an in vitro model of guinea pig primary gastric epithelial cells and fibroblasts treated with bacterial components: glycine acid extract (GE), urease subunit A (UreA), cytotoxin-associated gene A protein (CagA) and lipopolysaccharide (LPS). Cells were evaluated for metabolic activity (MTT reduction), myeloperoxidase (MPO) and metalloproteinase (MMP-9) secretion, lipid peroxidation (4-hydroxynonenal (4HNE)), migration (wound healing), proliferation (Ki-67 antigen) and cell apoptosis (TUNEL assay; Bcl-xL, Bax, Bcl-2 expression; caspase 3 cleavage).
resultsSignificant infiltration of the gastric mucosa by inflammatory cells in vivo in response to H. pylori was accompanied by oxidative stress and cell apoptosis, which were more intense 7 than 28 days after inoculation. The increase in cell proliferation was more intense in chronic than acute infection. H. pylori components GE, CagA, UreA, and LPS upregulated oxidative stress and apoptosis. Only H. pylori LPS inhibited cell migration and proliferation, which was accompanied by the upregulation of MMP-9.
conclusionsH. pylori infection induces cell apoptosis in conjunction with increased oxidative stress. Elevated apoptosis protects against deleterious inflammation and neoplasia; however, it reduces cell integrity. Upregulation of cell migration and proliferation in response to injury in the milieu of GE, CagA or UreA facilitates tissue regeneration but increases the risk of neoplasia. By comparison, downregulation of cell regeneration by H. pylori LPS may promote chronic inflammation.
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.