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.

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

MORBIATO, LAURA;TOMBOLA, FRANCESCO;ZORATTI, MARIO;PAPINI, EMANUELE
2001

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.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11577/2530413
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