ArticleInfection and immunity2001
Epithelial intestinal cell apoptosis induced by Helicobacter pylori depends on expression of the cag pathogenicity island phenotype.
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.
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Who cites it
23 citing papers in PubMed, 53 citations in OpenAlex.
- A vicious cycle inducer in gastric pathogenesis: implication of Helicobacter pylori.Archives of microbiology · 2026Review
- A Novel ProbioticMicrobiology spectrum · 2022Article
- The expression of RIPK3 is associated with cell turnover of gastric mucosa in the mouse and human stomach.Journal of molecular histology · 2021Article
- Role of caspase-3/E-cadherin in helicobacter pylori-induced apoptosis of gastric epithelial cells.Oncotarget · 2017Article
- Effect of Helicobacter pylori on gastric epithelial cells.World journal of gastroenterology · 2014Review
- Helicobacter pylori regulates iNOS promoter by histone modifications in human gastric epithelial cells.Medical microbiology and immunology · 2012Article
- Intestinal epithelial barrier dysfunction in food hypersensitivity.Journal of allergy · 2012Article
- Role of cagA-positive Helicobacter pylori on cell proliferation, apoptosis, and inflammation in biliary cells.Digestive diseases and sciences · 2011Article
- Interplay between Helicobacter pylori and immune cells in immune pathogenesis of gastric inflammation and mucosal pathology.Cellular & molecular immunology · 2010Review
- The significance of E266K polymorphism in the NOD1 gene on Helicobacter pylori infection: an effective force on pathogenesis?Clinical and experimental medicine · 2010Article
- The 3'-to-5' exoribonuclease (encoded by HP1248) of Helicobacter pylori regulates motility and apoptosis-inducing genes.Journal of bacteriology · 2009Article
- H. pylori-induced apoptosis in human gastric cancer cells mediated via the release of apoptosis-inducing factor from mitochondria.Helicobacter · 2008Article
- SGLT-1-mediated glucose uptake protects human intestinal epithelial cells against Giardia duodenalis-induced apoptosis.International journal for parasitology · 2008Article
- The effect of the cag pathogenicity island on binding of Helicobacter pylori to gastric epithelial cells and the subsequent induction of apoptosis.Helicobacter · 2007Article
- Helicobacter pylori infection induces oxidative stress and programmed cell death in human gastric epithelial cells.Infection and immunity · 2007Article
- Involvement of mast cells in gastritis caused by Helicobacter pylori: a potential role in epithelial cell apoptosis.Journal of clinical pathology · 2007Article
- Helicobacter pylori enhances tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in human gastric epithelial cells.World journal of gastroenterology · 2004Article
- Article
- Helicobacter pylori outer membrane vesicles modulate proliferation and interleukin-8 production by gastric epithelial cells.Infection and immunity · 2003Article
- Apoptosis of gastric lymphocytes in Helicobacter pylori-infected rhesus macaques.Digestive diseases and sciences · 2003Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori has been shown to induce chronic active gastritis and peptic ulcer and may contribute to the development of duodenal ulcer. Previous studies have shown that H. pylori mediates apoptosis of gastric epithelial cells via a Fas-dependent pathway. However, evidence for the induction of such a mechanism in intestinal epithelial cells (IEC) by H. pylori infection has not been demonstrated yet. This study was performed (i) to ascertain that H. pylori can induce IEC apoptosis; (ii) to delineate the role of the cag pathogenicity island (PAI), cagE, and vacA gene products in this process; and (iii) to verify whether the Fas-dependent pathway is involved in this phenomenon. When T84 cells were exposed to VacA(+)/cag PAI(+) H. pylori strains (CCUG 17874 and 60190), they exhibited apoptosis hallmarks as assessed by morphological studies, as well as annexin V and 3,3'-dihexyloxacarbocyanine iodide staining. In contrast, few or no apoptotic features could be detected after incubation with an isogenic mutant of strain 60190 in which the cagE gene was disrupted (60190:C(-) strain) or with a VacA(-)/cag PAI(-) H. pylori strain (G21). In addition, activation of caspase-3 during infection with VacA(+)/cag PAI(+) H. pylori strains was inhibited by pretreatment of IEC with an antagonistic anti-Fas antibody (ZB4). Taken together, these findings indicate that H. pylori triggers apoptosis in IEC via a Fas-dependent pathway following a process that depends on the expression of the cag PAI.
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