ArticleInfection and immunity2012
Comparative analysis of the interaction of Helicobacter pylori with human dendritic cells, macrophages, and monocytes.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
54 citing papers in PubMed, 109 citations in OpenAlex.
- Towards EffectiveInternational journal of molecular sciences · 2025Review
- Marine-Derived Fucose-Containing Carbohydrates: Review of Sources, Structure, and Beneficial Effects on Gastrointestinal Health.Foods (Basel, Switzerland) · 2024Review
- Helicobacter pylori disrupts gastric mucosal homeostasis by stimulating macrophages to secrete CCL3.Cell communication and signaling : CCS · 2024Article
- Current research on the interaction between Helicobacter pylori and macrophages.Molecular biology reports · 2024Review
- Notch Signaling Regulates the Function and Phenotype of Dendritic Cells inMicroorganisms · 2023Article
- Impact of intestinal microenvironments in obesity and bariatric surgery on shaping macrophages.Immunometabolism (Cobham, Surrey) · 2023Review
- Immune Biology and Persistence of Helicobacter pylori in Gastric Diseases.Current topics in microbiology and immunology · 2023Article
- Innate Immunity Crosstalk withInternational journal of molecular sciences · 2022Review
- The interplay betweenFrontiers in cellular and infection microbiology · 2022Review
- The role of non-coding RNA in the diagnosis and treatment ofFrontiers in medicine · 2022Review
- The Efficacy of Cancer Immunotherapies Is Compromised byFrontiers in immunology · 2022Review
- Article
- In Vitro Study of the Expression of CD1, CD14, CD25, CD30, CD35, CD95 Receptors by Macrophages of Mice Infected with Mycobacterium tuberculosis.Bulletin of experimental biology and medicine · 2021Article
- Overview ofDiseases (Basel, Switzerland) · 2021Review
- Innate Memory Reprogramming by Gold Nanoparticles Depends on the Microbial Agents That Induce Memory.Frontiers in immunology · 2021Article
- Notch Signaling Ligand Jagged1 Enhances Macrophage-Mediated Response toFrontiers in microbiology · 2021Article
- High Endothelin Receptor Type A Expression as an Independent Prognostic Biomarker and Correlated with Immune Infiltrates in Stomach Adenocarcinoma.Cancer management and research · 2021Article
- Contribution of Heptose Metabolites and theFrontiers in immunology · 2021Article
- H. pylori modulates DC functions via T4SS/TNFα/p38-dependent SOCS3 expression.Cell communication and signaling : CCS · 2020Article
- Immunological Aspects of the Tumor Microenvironment and Epithelial-Mesenchymal Transition in Gastric Carcinogenesis.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori may cause chronic gastritis, gastric cancer, or lymphoma. Myeloid antigen-presenting cells (APCs) are most likely involved in the induction and expression of the underlying inflammatory responses. To study the interaction of human APC subsets with H. pylori, we infected monocytes, monocyte-derived dendritic cells (DCs), and monocyte-derived (classically activated; M1) macrophages with H. pylori and analyzed phenotypic alterations, cytokine secretion, phagocytosis, and immunostimulation. Since we detected CD163(+) (alternatively activated; M2) macrophages in gastric biopsy specimens from H. pylori-positive patients, we also included monocyte-derived M2 macrophages in the study. Upon H. pylori infection, monocytes secreted interleukin-1β (IL-1β), IL-6, IL-10, and IL-12p40 (partially secreted as IL-23) but not IL-12p70. Infected DCs became activated, as shown by the enhanced expression of CD25, CD80, CD83, PDL-1, and CCR7, and secreted IL-1β, IL-6, IL-10, IL-12p40, IL-12p70, and IL-23. However, infection led to significantly downregulated CD209 and suppressed the constitutive secretion of macrophage migration inhibitory factor (MIF). H. pylori-infected M1 macrophages upregulated CD14 and CD32, downregulated CD11b and HLA-DR, and secreted mainly IL-1β, IL-6, IL-10, IL-12p40, and IL-23. Activation of DCs and M1 macrophages correlated with increased capacity to induce T-cell proliferation and decreased phagocytosis of dextran. M2 macrophages upregulated CD14 and CD206 and secreted IL-10 but produced less of the proinflammatory cytokines than M1 macrophages. Thus, H. pylori affects the functions of human APC subsets differently, which may influence the course and the outcome of H. pylori infection. The suppression of MIF in DCs constitutes a novel immune evasion mechanism exploited by H. pylori.
Indexed as
Identifiers
What OpenQuestion holds
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.