ArticleInfection and immunity2004
Helicobacter pylori induces apoptosis of macrophages in association with alterations in the mitochondrial pathway.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 86 citations in OpenAlex.
- Dysregulated macrophage immunity inFrontiers in immunology · 2025Review
- Vacuolating Cytotoxin A (VacA) and Extracellular Vesicles inIranian journal of pathology · 2025Review
- Changes in potential pathogenicity-associated proteins ofFrontiers in microbiology · 2025Article
- Helicobacter pylori infection and Parkinson's Disease: etiology, pathogenesis and levodopa bioavailability.Immunity & ageing : I & A · 2024Review
- Restoration of mitochondrial structure and function withinAdvances in microbiology · 2023Article
- Immune Biology and Persistence of Helicobacter pylori in Gastric Diseases.Current topics in microbiology and immunology · 2023Article
- Inflammatory microenvironment in gastric premalignant lesions: implication and application.Frontiers in immunology · 2023Review
- The Efficacy of Cancer Immunotherapies Is Compromised byFrontiers in immunology · 2022Review
- Upregulation of MUC5AC production and deposition of LEWIS determinants by HELICOBACTER PYLORI facilitate gastric tissue colonization and the maintenance of infection.Journal of biomedical science · 2019Article
- Potential risk factors and prevalence of Helicobacter pylori infection among adult patients with dyspepsia symptoms in Cameroon.BMC infectious diseases · 2018Article
- Comparative study of macrophages in naked mole rats and ICR mice.Oncotarget · 2017Article
- Fucosyltransferase-4 and Oligosaccharide Lewis Y Antigen as potentially Correlative Biomarkers of Helicobacter pylori CagA Associated Gastric Cancer.Pathology oncology research : POR · 2017Article
- Impact of Helicobacter pylori on the healing process of the gastric barrier.World journal of gastroenterology · 2016Article
- Review
- Morphological and Cellular Features of Innate Immune Reaction in Helicobacter pylori Gastritis: A Brief Review.International journal of molecular sciences · 2016Review
- Molecular and Proteomic Analysis of Levofloxacin and Metronidazole ResistantFrontiers in microbiology · 2016Article
- Suppression of cell division-associated genes by Helicobacter pylori attenuates proliferation of RAW264.7 monocytic macrophage cells.Scientific reports · 2015Article
- Helicobacter pylori and gastric cancer: a state of the art review.Gastroenterology and hepatology from bed to bench · 2015Review
- Heme oxygenase-1 dysregulates macrophage polarization and the immune response to Helicobacter pylori.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- H. pylori infection, inflammation and gastric cancer.Journal of gastrointestinal cancer · 2014Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori is a gastric bacterial pathogen that evades host immune responses in vivo and is associated with the development of gastritis, peptic ulcer disease, and gastric cancers. Induction of macrophage apoptosis is a method employed by multiple pathogens to escape host immune responses. Therefore, we hypothesized that H. pylori induces apoptosis of infected macrophages. RAW 264.7 cells were infected with H. pylori strain 60190, and apoptosis was assessed. Transmission electron microscopy and fluorescence microscopy showed that infected macrophages displayed morphological features characteristic of apoptosis. Quantification by acridine orange-ethidium bromide fluorescent-dye staining showed that apoptosis was dose and time dependent, and apoptosis was further confirmed by increased binding of annexin V-fluorescein isothiocyanate (FITC) to externalized phosphatidylserine of infected but not of control macrophages. Macrophages infected with isogenic mutants of H. pylori strain 60190 deficient in either cagA or vacA induced significantly less apoptosis than the parental strain, as assessed by increased binding of annexin V-FITC. Western blot analysis of whole-cell protein lysates revealed that infection with strain 60190 induced a time-dependent increase in cleavage of procaspase 8 and disappearance of full-length Bid compared with uninfected cells. Furthermore, pharmacological inhibition of caspase 8 caused a decrease in levels of apoptosis. Finally, infection caused a time-dependent increase in mitochondrial-membrane permeability and release of cytochrome c into the cytosol. These results suggest that H. pylori induces apoptosis of macrophages in association with alterations in the mitochondrial pathway. Elimination of this key immunomodulatory cell may represent a mechanism employed by the bacterium to evade host immune responses.
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