ArticleThe Journal of experimental medicine2000
Virulent strains of Helicobacter pylori demonstrate delayed phagocytosis and stimulate homotypic phagosome fusion in macrophages.
Article in The Journal of experimental medicine, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 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.
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.
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Who cites it
83 citing papers in PubMed, 213 citations in OpenAlex.
- Helicobacter pylori cholesteryl α-glucosides contribute to its pathogenicity and immune response by natural killer T cells.PloS one · 2013Trial
- Co-infection ofJournal of virology · 2025Article
- Dysregulated macrophage immunity inFrontiers in immunology · 2025Review
- Review
- Article
- Innate Immunity Crosstalk withInternational journal of molecular sciences · 2022Review
- Single-phagosome imaging reveals that homotypic fusion impairs phagosome degradative function.Biophysical journal · 2022Article
- The Efficacy of Cancer Immunotherapies Is Compromised byFrontiers in immunology · 2022Review
- Vitamin DFrontiers in microbiology · 2022Article
- An Overview of Autophagy inFrontiers in cellular and infection microbiology · 2022Review
- Helicobacter pylori-derived outer membrane vesicles stimulate interleukin 8 secretion through nuclear factor kappa B activation.The Korean journal of internal medicine · 2021Article
- Innate Memory Reprogramming by Gold Nanoparticles Depends on the Microbial Agents That Induce Memory.Frontiers in immunology · 2021Article
- Microtubules and Dynein Regulate Human Neutrophil Nuclear Volume and Hypersegmentation DuringFrontiers in immunology · 2021Article
- Encephalitozoon cuniculi takes advantage of efferocytosis to evade the immune response.PloS one · 2021Article
- H. pylori infection confers resistance to apoptosis via Brd4-dependent BIRC3 eRNA synthesis.Cell death & disease · 2020Article
- B-1 cell-mediated modulation of M1 macrophage profile ameliorates microbicidal functions and disrupt the evasion mechanisms of Encephalitozoon cuniculi.PLoS neglected tropical diseases · 2019Article
- Vitamin D3 activates the autolysosomal degradation function against Helicobacter pylori through the PDIA3 receptor in gastric epithelial cells.Autophagy · 2019Article
- Article
- Article
- Helicobacter pylori Deregulates T and B Cell Signaling to Trigger Immune Evasion.Current topics in microbiology and immunology · 2019Review
23 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Helicobacter pylori colonizes the gastric epithelium of approximately 50% of the world's population and plays a causative role in the development of gastric and duodenal ulcers. H. pylori is phagocytosed by mononuclear phagocytes, but the internalized bacteria are not killed and the reasons for this host defense defect are unclear. We now show using immunofluorescence and electron microscopy that H. pylori employs an unusual mechanism to avoid phagocytic killing: delayed entry followed by homotypic phagosome fusion. Unopsonized type I H. pylori bound readily to macrophages and were internalized into actin-rich phagosomes after a lag of approximately 4 min. Although early (10 min) phagosomes contained single bacilli, H. pylori phagosomes coalesced over the next approximately 2 h. The resulting "megasomes" contained multiple viable organisms and were stable for 24 h. Phagosome-phagosome fusion required bacterial protein synthesis and intact host microtubules, and both chloramphenicol and nocodazole increased killing of intracellular H. pylori. Type II strains of H. pylori are less virulent and lack the cag pathogenicity island. In contrast to type I strains, type II H. pylori were rapidly ingested and killed by macrophages and did not stimulate megasome formation. Collectively, our data suggest that megasome formation is an important feature of H. pylori pathogenesis.
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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.