Candida albicans Inhibits Pseudomonas aeruginosa Virulence through Suppression of Pyochelin and Pyoverdine Biosynthesis.

Détails

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Etat: Serval
Version: de l'auteur
ID Serval
serval:BIB_9AACA2033D8B
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Candida albicans Inhibits Pseudomonas aeruginosa Virulence through Suppression of Pyochelin and Pyoverdine Biosynthesis.
Périodique
Plos Pathogens
Auteur(s)
Lopez-Medina E., Fan D., Coughlin L.A., Ho E.X., Lamont I.L., Reimmann C., Hooper L.V., Koh A.Y.
ISSN
1553-7374 (Electronic)
ISSN-L
1553-7366
Statut éditorial
Publié
Date de publication
2015
Peer-reviewed
Oui
Volume
11
Numéro
8
Pages
e1005129
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't Publication Status: epublish
Résumé
Bacterial-fungal interactions have important physiologic and medical ramifications, but the mechanisms of these interactions are poorly understood. The gut is host to trillions of microorganisms, and bacterial-fungal interactions are likely to be important. Using a neutropenic mouse model of microbial gastrointestinal colonization and dissemination, we show that the fungus Candida albicans inhibits the virulence of the bacterium Pseudomonas aeruginosa by inhibiting P. aeruginosa pyochelin and pyoverdine gene expression, which plays a critical role in iron acquisition and virulence. Accordingly, deletion of both P. aeruginosa pyochelin and pyoverdine genes attenuates P. aeruginosa virulence. Heat-killed C. albicans has no effect on P. aeruginosa, whereas C. albicans secreted proteins directly suppress P. aeruginosa pyoverdine and pyochelin expression and inhibit P. aeruginosa virulence in mice. Interestingly, suppression or deletion of pyochelin and pyoverdine genes has no effect on P. aeruginosa's ability to colonize the GI tract but does decrease P. aeruginosa's cytotoxic effect on cultured colonocytes. Finally, oral iron supplementation restores P. aeruginosa virulence in P. aeruginosa and C. albicans colonized mice. Together, our findings provide insight into how a bacterial-fungal interaction can modulate bacterial virulence in the intestine. Previously described bacterial-fungal antagonistic interactions have focused on growth inhibition or colonization inhibition/modulation, yet here we describe a novel observation of fungal-inhibition of bacterial effectors critical for virulence but not important for colonization. These findings validate the use of a mammalian model system to explore the complexities of polymicrobial, polykingdom infections in order to identify new therapeutic targets for preventing microbial disease.
Mots-clé
Animals, Candida albicans/physiology, Farnesol/pharmacology, Female, Gastrointestinal Tract/microbiology, Iron/metabolism, Male, Mice, Mice, Inbred C3H, Oligopeptides/antagonists & inhibitors, Oligopeptides/biosynthesis, Phenols/antagonists & inhibitors, Pseudomonas aeruginosa/pathogenicity, Thiazoles/antagonists & inhibitors, Virulence
Pubmed
Web of science
Création de la notice
29/09/2015 17:39
Dernière modification de la notice
03/03/2018 19:52
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