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Activation of proinflammatory response in human intestinal epithelial cells following Vibrio cholerae infection through PI3K/Akt pathway

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Vibrio cholerae activates proinflammatory response in cultured intestinal epithelial cells. In this study, we demonstrate that V. cholerae O395 infection of intestinal epithelial cells results in the activation of Akt. Inhibition of Akt significantly decreases IL-1α, IL-6, and TNF-α production in V. cholerae infected Int407 cells. Analysis of the mechanisms of Akt influences on cytokine response demonstrates that Akt promotes NF-B activation. We have extended these findings to show that Akt activation may be regulated by bacterial genes associated with virulence, adherence, or motility. Insertion mutants in the virulence genes coding for CtxA, ToxT, and OmpU of V. cholerae modulate the activation of PI3K/Akt signaling pathway, whereas an aflagellate non-motile mutant (O395FLAN) and a adherent and less motile mutant (O395Y3N/O395Y4N) of V. cholerae both show very significant down-regulation of Akt activity in Int407 cells. Together, these observations indicate that Akt promotes proinflammatory cytokine production by V. cholerae infected human intestinal epithelial cells through its influences on NF-B.

Vibrio cholerae active la réponse pro-inflammatoire des cellules épithéliales de l’intestin en culture. Dans cette étude, nous démontrons qu’Akt est activée chez les cellules épithéliales de l’intestin infectées à V. cholerae O395. L’inhibition d’Akt diminue significativement la production d’IL-1α, d’IL-6 et de TNF-α par les cellules Int407 infectées par V. cholerae. L’analyse des mécanismes responsables de l’action d’Akt sur la production de cytokines démontre qu’Akt favorise l’activation de NF-B. Nous avons poussé plus loin ces conclusions pour montrer que l’activation d’Akt peut être régulée par des gènes bactériens associés à la virulence, l’adhérence ou la motilité. Des mutants d’insertion des gènes de virulence CtxA, ToxT et OmpU de V. cholerae affectent la voie de signalisation PI3K/Akt. L’activation d’Akt est moindre chez les cellules Int407 infectées avec le mutant O395FLAN, non motile et sans flagelle, ou avec le mutant O395Y3N/O395Y4N dont la motilité et l’adhérence sont diminuées. En somme, ces observation indiquent qu’Akt favorise la production de cytokines proinflammatoires chez les cellules épithéliales de l’intestin infectées par V. cholerea via son influence sur NF-B.

Document Type: Research Article

Publication date: 2009-11-01

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  • Published since 1954, this monthly journal contains new research in the field of microbiology including applied microbiology and biotechnology; microbial structure and function; fungi and other eucaryotic protists; infection and immunity; microbial ecology; physiology, metabolism and enzymology; and virology, genetics, and molecular biology. It also publishes review articles and notes on an occasional basis, contributed by recognized scientists worldwide.
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