Vacuolation induced by VacA toxin of Helicobacter pylori requires the intracellular accumulation of membrane permeant bases, Cl- and water

Laura Morbiato, Francesco Tombola, Silvia Campello, Giuseppe Del Giudice, Rino Rappuoli, Mario Zoratti, Emanuele Papini

Research output: Contribution to journalArticlepeer-review

Abstract

The protein vacuolating toxin A (VacA) of Helicobacter pylori converts late endosomes into large vacuoles in the presence of permeant bases. Here it is shown that this phenomenon corresponds to an accumulation of permeant bases and Cl- in HeLa cells and requires the presence of extracellular Cl-. The net influx of Cl- is due to electroneutral, Na+, K+, 2Cl- cotransporter-mediated transport. Cell vacuolation leads to cell volume increase, consistent with water flux into the cell, while hyper-osmotic media decreased vacuole formation. These data represent the first evidence that VacA-treated cells undergo an osmotic unbalance, reinforcing the hypothesis that the VacA chloride channel is responsible for cell vacuolation.

Original languageEnglish
Pages (from-to)479-483
Number of pages5
JournalFEBS Letters
Volume508
Issue number3
DOIs
Publication statusPublished - Nov 23 2001

Keywords

  • Cell vacuolation
  • Cl transport
  • Helicobacter pylori
  • Na, K, 2Cl cotransporter
  • VacA anion channel

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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