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Helicobacter pylori enter and survive within multivesicular vacuoles of epithelial cells

Manuel R Amieva1, Nina R Salama, Lucy S Tompkins

  • 1Department of Microbiology and Immunology, Stanford University School of Medicine, 299 Campus Drive, Stanford, CA 94305, USA. amieva@stanford.edu

Cellular Microbiology
|October 9, 2002
PubMed

Insights

Helicobacter pylori can survive inside epithelial cells by entering large vacuoles, remaining viable and motile. This intracellular survival in a vacuolar niche may explain why H. pylori infections are difficult to eradicate.

Area of Science:

  • Microbiology
  • Cell Biology
  • Infectious Diseases

Background:

  • Intracellular Helicobacter pylori have been observed, but their fate and survival mechanisms remain unclear.
  • Understanding H. pylori's intracellular behavior is crucial for developing effective eradication strategies.

Purpose of the Study:

  • To investigate the fate and survival of intracellular Helicobacter pylori within host epithelial cells.
  • To elucidate the cellular mechanisms and niche exploited by H. pylori for intracellular survival.

Main Methods:

  • Utilized differential interference contrast (DIC) video and immunofluorescence microscopy to observe H. pylori within cells.
  • Employed time-lapse microscopy and pulsed gentamicin treatments to track bacterial viability and survival over time.
  • Used electron microscopy and endosomal dye staining to characterize the morphology of H. pylori-containing vacuoles.

Main Results:

  • A proportion of cell-associated H. pylori enter large cytoplasmic vacuoles in various epithelial cell lines.
  • Intravacuolar H. pylori remain viable, motile, and protected from extracellular gentamicin, with a half-life of approximately 24 hours.
  • These vacuoles resemble late endosomal multivesicular bodies, and bacterial entry/survival is independent of VacA.

Conclusions:

  • Helicobacter pylori exploits an intravacuolar niche within host epithelial cells for survival.
  • This intracellular survival mechanism, involving vacuole formation and protection, contributes to the persistence and difficulty in eradicating H. pylori infections.

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