ArticleCurrent microbiology2006
Helicobacter pylori induces apoptosis of T- and B-cell lines and translocates mitochondrial apoptosis-inducing factor to nucleus.
Article in Current microbiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 16 citations in OpenAlex.
- miR-136: A biomarker in the inflammation-cancer transformation of gastric cancer.World journal of gastrointestinal oncology · 2025Article
- Programmed cell death inFrontiers in cellular and infection microbiology · 2024Review
- Poly(ADP-Ribose) Polymerases in Host-Pathogen Interactions, Inflammation, and Immunity.Microbiology and molecular biology reviews : MMBR · 2019Review
- Pathogen manipulation of B cells: the best defence is a good offence.Nature reviews. Microbiology · 2015Review
- B lymphocytes undergo TLR2-dependent apoptosis upon Shigella infection.The Journal of experimental medicine · 2014Article
- Low-density lipoprotein receptor-related protein-1 (LRP1) mediates autophagy and apoptosis caused by Helicobacter pylori VacA.The Journal of biological chemistry · 2012Article
- Helicobacter pylori vacuolating toxin A and apoptosis.Cell communication and signaling : CCS · 2011Article
- Activation of the abundant nuclear factor poly(ADP-ribose) polymerase-1 by Helicobacter pylori.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Helicobacter pylori is invasive and it may be a facultative intracellular organism.Cellular microbiology · 2007Review
- Helicobacter pylori activation of PARP-1: usurping a versatile regulator of host cellular health.Gut microbesReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immune cell apoptosis may play a role in human persistent Helicobacter pylori infection. We planned to study the apoptosis of T and B cells by H. pylori strains. T (Jurkat) and B (Raji) cell lines were co-cultured with cagA-positive H. pylori strains carrying different vacA genotypes (s1a/m1, s1a/m2, and s2/m2). Apoptosis was detected by microscopy, DNA fragmentation assay, and flow cytometry. Apoptosis-inducing factor (AIF) transfer from mitochondria to nucleus was studied by immunoblot analysis. Apoptosis of T and B cells was significantly higher in H. pylori-infected cells than in uninfected controls (s1a/m1 80%, s1a/m2 78%, s2m2 69% vs. control 16% for T cells, P < 0.001; s1 a/m1 78%, s1a/m2 73%, s2m2 62% vs. control 24% for B cells, P < 0.001 by flow cytometry) with no difference among the genotypes. AIF transfer from mitochondria to nucleus was demonstrated in both apoptotic cell lines. Thus, H. pylori induces apoptosis in T- and B-cell lines and translocates AIF. T and B cells deletion through apoptosis may explain the persistence of H. pylori infection; its role in pathogenesis needs further research.
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