Evidence map›Paper›PMID 36792546›Full record

ArticleJournal of extracellular vesicles2023

Helicobacter pylori-derived outer membrane vesicles contribute to Alzheimer's disease pathogenesis via C3-C3aR signalling.

Junhua Xie, Lien Cools, Griet Van Imschoot, Elien Van Wonterghem, Marie J Pauwels, Ine Vlaeminck, Chloë De Witte, Samir El Andaloussi, Keimpe Wierda, Lies De Groef and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of extracellular vesicles, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 1 pooled it
22.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

100 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. Pooled it
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  18. Characterization ofMicroorganisms · 2026
    Article
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40 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 1 institution in 2 countries.

Junhua XieVIB Center for Inflammation Research, VIB, Ghent, Belgium.ORCID 0000-0003-0684-8515
Lien CoolsVIB Center for Inflammation Research, VIB, Ghent, Belgium.
Griet Van ImschootVIB Center for Inflammation Research, VIB, Ghent, Belgium.
Elien Van WonterghemVIB Center for Inflammation Research, VIB, Ghent, Belgium.
Marie J PauwelsVIB Center for Inflammation Research, VIB, Ghent, Belgium.
Ine VlaeminckVIB Center for Brain & Disease Research, Electrophysiology Expertise Unit, Leuven, Belgium.ORCID 0000-0001-8934-6179
Chloë De WitteDepartment of Pathobiology, Pharmacology and Zoological Medicine, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium.
Samir El AndaloussiDepartment of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
Keimpe WierdaVIB Center for Brain & Disease Research, Electrophysiology Expertise Unit, Leuven, Belgium.ORCID 0000-0002-8784-9490
Lies De GroefCellular Communication and Neurodegeneration Research Group, Department of Biology, Leuven Brain Institute, KU Leuven, Leuven, Belgium.ORCID 0000-0002-3329-3474
Freddy HaesebrouckDepartment of Pathobiology, Pharmacology and Zoological Medicine, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium.ORCID 0000-0002-1709-933X
Lien Van HoeckeVIB Center for Inflammation Research, VIB, Ghent, Belgium.ORCID 0000-0001-8602-4211
Roosmarijn E VandenbrouckeVIB Center for Inflammation Research, VIB, Ghent, Belgium.ORCID 0000-0002-8327-620X
Ghent University Hospital · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The gut microbiota represents a diverse and dynamic population of microorganisms that can influence the health of the host. Increasing evidence supports the role of the gut microbiota as a key player in the pathogenesis of neurodegenerative diseases, including Alzheimer's disease (AD). Unfortunately, the mechanisms behind the interplay between gut pathogens and AD are still elusive. It is known that bacteria-derived outer membrane vesicles (OMVs) act as natural carriers of virulence factors that are central players in the pathogenesis of the bacteria. Helicobacter pylori (H. pylori) is a common gastric pathogen and H. pylori infection has been associated with an increased risk to develop AD. Here, we are the first to shed light on the role of OMVs derived from H. pylori on the brain in healthy conditions and on disease pathology in the case of AD. Our results reveal that H. pylori OMVs can cross the biological barriers, eventually reaching the brain. Once in the brain, these OMVs are taken up by astrocytes, which induce activation of glial cells and neuronal dysfunction, ultimately leading to exacerbated amyloid-β pathology and cognitive decline. Mechanistically, we identified a critical role for the complement component 3 (C3)-C3a receptor (C3aR) signalling in mediating the interaction between astrocytes, microglia and neurons upon the presence of gut H. pylori OMVs. Taken together, our study reveals that H. pylori has a detrimental effect on brain functionality and accelerates AD development via OMVs and C3-C3aR signalling.

Indexed as

Alzheimer DiseaseExtracellular VesiclesHelicobacter pyloriBrainComplement C3HumansReceptors, ComplementC3 protein, humanComplement C3complement C3a receptorReceptors, ComplementAlzheimer's diseasebacterial extracellular vesicles (bEVs)C3complementgut-brain axisHelicobacter pyloriouter membrane vesicles (OMVs)

Identifiers

PMID36792546
PMCPMC9931688
OpenAlexW4320884661

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.