ArticleMediators of inflammation2015
Helicobacter pylori outer membrane vesicle proteins induce human eosinophil degranulation via a β2 Integrin CD11/CD18- and ICAM-1-dependent mechanism.
Article in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 25 citations in OpenAlex.
- Beyond the Stomach: Exploring the Role ofExpert reviews in molecular medicine · 2026Review
- Helicobacter pylori-derived outer membrane vesicles: Pathogenic roles, microbiota interactions, and biomedical applications.Journal of advanced research · 2026Review
- Integrated transcriptomics and molecular docking identify hub genes and statin regulators inFrontiers in cellular and infection microbiology · 2026Article
- Review
- Eosinophils as drivers of bacterial immunomodulation and persistence.Infection and immunity · 2024Review
- Review
- Review
- Emerging role of microbiota derived outer membrane vesicles to preventive, therapeutic and diagnostic proposes.Infectious agents and cancer · 2023Review
- Outer Membrane Vesicles Secreted byACS omega · 2022Article
- Review
- Outer membrane vesicles for vaccination and targeted drug delivery.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology · 2019Review
- Bacterial outer membrane vesicles, a potential vaccine candidate in interactions with host cells based.Diagnostic pathology · 2018Review
- Helicobacter pylori outer membrane vesicles involvement in the infection development and Helicobacter pylori-related diseases.Journal of biomedical science · 2018Review
- Role of microRNAs and Exosomes inFrontiers in microbiology · 2018Review
- Role of Leptin/Osteopontin Axis in the Function of Eosinophils in Allergic Rhinitis with Obesity.Mediators of inflammation · 2018Article
- Crude Preparations of Helicobacter pylori Outer Membrane Vesicles Induce Upregulation of Heme Oxygenase-1 via Activating Akt-Nrf2 and mTOR-IκB Kinase-NF-κB Pathways in Dendritic Cells.Infection and immunity · 2016Article
- A Player and Coordinator: The Versatile Roles of Eosinophils in the Immune System.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Eosinophil cationic protein (ECP), a cytotoxic protein contained in eosinophils granules, can contribute to various inflammatory responses. Although Helicobacter pylori infection increases infiltration of eosinophils, the mechanisms of eosinophil degranulation by H. pylori infection are largely unknown. The goal of this study was to investigate the role of H. pylori outer membrane vesicles (OMVs) in modulating eosinophil degranulation. We found that eosinophils treated with H. pylori OMVs released significantly more ECP compared with untreated controls. In addition, eosinophils cocultured with OMV-preexposed primary gastric epithelial cells exhibited significantly increased ECP release. Similarly, eosinophils cocultured with culture supernatant (CM) from primary gastric epithelial cells exposed to OMVs (OMV-CM) released significantly higher amounts of ECP compared with eosinophils cocultured with CM from unexposed control cells. Furthermore, OMVs and OMV-CM both induced the upregulation of ICAM-1 on gastric epithelial cells and β2 integrin CD11b on eosinophils. In addition, both transduction of ICAM-1 shRNA into gastric epithelial cells and treatment with neutralizing mAbs to CD18 significantly decreased OMV-mediated or OMV-CM-mediated release of ECP. These results suggest that the eosinophil degranulation response to H. pylori OMVs occurs via a mechanism that is dependent on both β2 integrin CD11/CD18 and ICAM-1.
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.