ArticleDigestive diseases and sciences2008
Disturbance of apoptosis and DNA synthesis by Helicobacter pylori infection of hepatocytes.
Article in Digestive diseases and sciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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.
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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.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- A model of Helicobacter infection using an artificial liver constructed by a radial-flow bioreactor.Human cell · 2026Article
- Effects and mechanisms ofWorld journal of gastroenterology · 2024Review
- The interplay between Helicobacter pylori infection and rs738409 PNPLA3 in metabolic dysfunction-associated steatotic liver disease.PloS one · 2024Article
- Cortactin Promotes Effective AGS Cell Scattering byPathogens (Basel, Switzerland) · 2021Article
- Microbes in Tumoral In Situ Tissues and in Tumorigenesis.Frontiers in cellular and infection microbiology · 2020Review
- Review
- Article
- The Association between Helicobacter pylori Infection and Chronic Hepatitis C: A Meta-Analysis and Trial Sequential Analysis.Gastroenterology research and practice · 2016Review
- From the stomach to other organs: Helicobacter pylori and the liver.World journal of hepatology · 2015Review
- Comparative genomic study of gastric epithelial cells co-cultured with Helicobacter pylori.World journal of gastroenterology · 2012Article
- Effects of Helicobacter pylori γ-glutamyltranspeptidase on apoptosis and inflammation in human biliary cells.Digestive diseases and sciences · 2012Article
- Interleukin-8 is the single most up-regulated gene in whole genome profiling of H. pylori exposed gastric epithelial cells.BMC microbiology · 2012Article
- Role of cagA-positive Helicobacter pylori on cell proliferation, apoptosis, and inflammation in biliary cells.Digestive diseases and sciences · 2011Article
- Hypothesis: TargetedHepatic medicine : evidence and research · 2010Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
We evaluated the effects of infection of hepatocytes with the well-characterized Helicobacter species, H. pylori. Cell number doubled during each 24 h period in mock cultures or following infection with H. pylori 401C (CagA-, VacA-, BabA-, OipA-) (P < 0.05). In contrast, infection with the more virulent H. pylori NCTC11637 (CagA+, VacA+, BabA+, OipA+) resulted in cell arrest (P < 0.05). Furthermore, NCTC11637 activated caspase-3 and increased DNA fragmentation 6.1 +/- 1.2 fold (P < 0.01) and the number of apoptotic bodies 9.4 +/- 3.5 fold (P < 0.01) compared to controls. The effect was greater than with the less virulent strain 401C (3.8 +/- 0.6 fold and 3.9 +/- 1.7, respectively, P < 0.05). Strain NCTC11637 at low concentrations increased cellular DNA synthesis 139 +/- 6% (P < 0.05) but decreased it to 16 +/- 7% (P < 0.01) at high concentrations. In contrast, strain 401C increased DNA synthesis 155 +/- 14% of controls (P < 0.05) at high concentrations. The presence of intracellular NCTC11637 within hepatocytes increased DNA fragmentation 3.0 +/- 0.4 fold (P < 0.01) greater than in controls. H. pylori infection resulted in strain-species-dependent effects on hepatocytes, and virulent strain caused cell arrest and apoptosis of infected hepatocytes.
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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.