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Updated: Aug 9, 2025

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

Junhua Xie1,2,3, Lien Cools1,2,4, Griet Van Imschoot1,2

  • 1VIB Center for Inflammation Research, VIB, Ghent, Belgium.

Journal of Extracellular Vesicles
|February 15, 2023
PubMed

Insights

Helicobacter pylori outer membrane vesicles (OMVs) can reach the brain, activating glial cells and worsening Alzheimer's disease (AD) pathology. This occurs via C3-C3aR signaling, highlighting a gut-brain axis link in AD pathogenesis.

Area of Science:

  • Neuroscience
  • Microbiology
  • Immunology

Background:

  • The gut microbiota influences host health, with increasing evidence linking it to neurodegenerative diseases like Alzheimer's disease (AD).
  • Bacteria-derived outer membrane vesicles (OMVs) are key virulence factors, and Helicobacter pylori (H. pylori) infection is associated with increased AD risk.
  • Mechanisms connecting gut pathogens to AD pathogenesis remain largely unknown.

Purpose of the Study:

  • To investigate the role of H. pylori OMVs in brain health and Alzheimer's disease (AD) pathology.
  • To elucidate the pathways by which H. pylori OMVs impact the brain.

Main Methods:

  • Investigated the ability of H. pylori OMVs to cross biological barriers and reach the brain.
  • Examined the uptake of OMVs by brain cells, specifically astrocytes.
  • Assessed the effects of OMVs on glial cell activation, neuronal function, and amyloid-beta pathology.
  • Analyzed the involvement of complement component 3 (C3)-C3a receptor (C3aR) signaling.

Main Results:

  • H. pylori OMVs were found to cross biological barriers and enter the brain.
  • OMV uptake by astrocytes led to glial cell activation and neuronal dysfunction.
  • H. pylori OMVs exacerbated amyloid-beta pathology and cognitive decline.
  • C3-C3aR signaling was identified as critical for mediating interactions between astrocytes, microglia, and neurons.

Conclusions:

  • H. pylori OMVs exert detrimental effects on brain function and accelerate AD development.
  • The study reveals a novel mechanism involving OMVs and C3-C3aR signaling in the gut-brain axis contributing to AD pathogenesis.
Keywords:
Helicobacter pyloriAlzheimer's diseaseC3bacterial extracellular vesicles (bEVs)complementgut-brain axisouter membrane vesicles (OMVs)

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