ArticleInfection and immunity2001
Apoptotic signaling pathway activated by Helicobacter pylori infection and increase of apoptosis-inducing activity under serum-starved conditions.
Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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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Who cites it
23 citing papers in PubMed, 55 citations in OpenAlex.
- Review
- From pyroptosis, apoptosis and necroptosis to PANoptosis: A mechanistic compendium of programmed cell death pathways.Computational and structural biotechnology journal · 2021Review
- Pathogen-induced ubiquitin-editing enzyme A20 bifunctionally shuts off NF-κB and caspase-8-dependent apoptotic cell death.Cell death and differentiation · 2017Article
- Role of caspase-3/E-cadherin in helicobacter pylori-induced apoptosis of gastric epithelial cells.Oncotarget · 2017Article
- Oral glutathione supplementation drastically reduces Helicobacter-induced gastric pathologies.Scientific reports · 2016Article
- Description of the interaction between Candida albicans and macrophages by mixed and quantitative proteome analysis without isolation.AMB Express · 2015Article
- Helicobacter pylori modulates host cell survival regulation through the serine-threonine kinase, 3-phosphoinositide dependent kinase 1 (PDK-1).BMC microbiology · 2015Article
- Article
- Helicobacter pylori gamma-glutamyltranspeptidase induces cell cycle arrest at the G1-S phase transition.Journal of microbiology (Seoul, Korea) · 2010Article
- H. pylori-induced apoptosis in human gastric cancer cells mediated via the release of apoptosis-inducing factor from mitochondria.Helicobacter · 2008Article
- Helicobacter pylori infection induces oxidative stress and programmed cell death in human gastric epithelial cells.Infection and immunity · 2007Article
- Serum-free culture of H pylori intensifies cytotoxicity.World journal of gastroenterology · 2007Article
- Helicobacter pylori induces apoptosis of T- and B-cell lines and translocates mitochondrial apoptosis-inducing factor to nucleus.Current microbiology · 2006Article
- Streptococcal pyrogenic exotoxin B-induced apoptosis in a549 cells is mediated by a receptor- and mitochondrion-dependent pathway.Infection and immunity · 2004Article
- Helicobacter pylori infection and gastric cancer: host, bug, environment, or all three?Current gastroenterology reports · 2004Review
- Prominent role of gamma-glutamyl-transpeptidase on the growth of Helicobacter pylori.World journal of gastroenterology · 2004Article
- Article
- Helicobacter pylori induces apoptosis of macrophages in association with alterations in the mitochondrial pathway.Infection and immunity · 2004Article
- Effect of Helicobacter pylori infection on expression of Bcl-2 family members in gastric adenocarcinoma.World journal of gastroenterology · 2004Article
- Nuclear factor kappa B protects against host cell apoptosis during Rickettsia rickettsii infection by inhibiting activation of apical and effector caspases and maintaining mitochondrial integrity.Infection and immunity · 2003Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The enhanced gastric epithelial cell apoptosis observed during infection with Helicobacter pylori has been suggested to be of significance in the etiology of gastritis, peptic ulcers, and neoplasia. To investigate the cell death signaling induced by H. pylori infection, human gastric epithelial cells were incubated with H. pylori for up to 72 h. H. pylori infection induced the activation of caspase -8, -9, and -3 and the expression of the proapoptotic Bcl-2 family proteins Bad and Bid. The peak of the activity of the caspases occurred at 24 h. At this time, the inhibition of caspase-8 or -9 almost completely suppressed H. pylori-induced apoptosis. Inhibition of caspase-8 suppressed the expression of Bad and Bid and the subsequent activation of caspase-9 and -3. These observations indicate that H. pylori induces apoptosis through a pathway involving the sequential induction of apical caspase-8 activity, the proapoptotic proteins Bad and Bid, caspase-9 activity, and effector caspase-3 activity. Activation of the pathway was independent of CagA or vacuolating toxin. A membrane fraction of H. pylori was sufficient to activate this pathway, and treatment with proteinase K eliminated the activity. Apoptotic activity of the membrane fraction was significantly increased by incubating the bacteria under serum-starved conditions for 24 h. These observations suggest that environmental conditions in the human stomach could induce H. pylori-mediated pathogenesis, leading to a variety of clinical outcomes.
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Registered trials
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