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Vacuolating cytotoxin of helicobacter pylori induces apoptosis in the human gastric epithelial cell line AGS

Helicobacter pylori induces cell death by apoptosis. However, the apoptosis-inducing factor is still unknown. The virulence factor vacuolating cytotoxin A (VacA) is a potential candidate, and thus its role in apoptosis induction was investigated in the human gastric epithelial cell line AGS. The sup...

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Hauptverfasser: Kuck, Dirk (VerfasserIn) , Krammer, Peter H. (VerfasserIn) , Stremmel, Wolfgang (VerfasserIn) , Rudi, Jochen (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: August 1, 2001
In: Infection and immunity
Year: 2001, Jahrgang: 69, Heft: 8, Pages: 5080-5087
ISSN:1098-5522
DOI:10.1128/IAI.69.8.5080-5087.2001
Online-Zugang:Verlag, Volltext: https://doi.org/10.1128/IAI.69.8.5080-5087.2001
Verlag, Volltext: https://iai.asm.org/content/69/8/5080
Volltext
Verfasserangaben:Dirk Kuck, Bernhard Kolmerer, Christof Iking-Konert, Peter H. Krammer, Wolfgang Stremmel, and Jochen Rudi
Beschreibung
Zusammenfassung:Helicobacter pylori induces cell death by apoptosis. However, the apoptosis-inducing factor is still unknown. The virulence factor vacuolating cytotoxin A (VacA) is a potential candidate, and thus its role in apoptosis induction was investigated in the human gastric epithelial cell line AGS. The supernatant from thevacA wild-type strain P12 was able to induce apoptotic cell death, whereas the supernatant from its isogenic mutant strain P14 could not. That VacA was indeed the apoptosis-inducing factor was demonstrated further by substantial reduction of apoptosis upon treatment of AGS cells with a supernatant specifically depleted of native VacA. Furthermore, a recombinant VacA produced inEscherichia coli was also able to induce apoptosis in AGS cells but failed to induce cellular vacuolation. These findings demonstrate that the vacuolating cytototoxin of H. pyloriis a bacterial factor capable of inducing apoptosis in gastric epithelial cells.
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Beschreibung:Online Resource
ISSN:1098-5522
DOI:10.1128/IAI.69.8.5080-5087.2001

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