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ID 56688
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Elgaml, Abdelaziz Graduate School of Medicine, Dentistry and Pharmaceutical SciencesOkayama University
Higaki, Kazutaka Graduate School of Medicine, Dentistry and Pharmaceutical SciencesOkayama University
Miyoshi, Shin-ichi Graduate School of Medicine, Dentistry and Pharmaceutical SciencesOkayama University
Abstract
Vibrio vulnificus is a halophilic estuarine bacterium while it causes fatal septicemia or necrotizing wound infections in humans. This pathogen secretes the metalloprotease (V. vulnificus protease: VVP) and the cytolysin (V. vulnificus hemolysin: VVH) as protein toxins; however, their production was coordinated in response to the bacterial cell density. This regulation is termed quorum sensing (QS) and is mediated by the small diffusible molecule called autoinducer 2 (AI-2). In the present study, we investigated effects of disruption of luxO encoding a central response regulator of the QS circuit, as well as effects of temperature and growth phase, on the toxin production by V. vulnificus. Disruption of luxO was found to increase VVP production and expression of its gene vvpE. The expression of smcR, crp and rpoS, of which products positively regulate vvpE expression, and luxS encoding the AI-2 synthetase were also significantly increased. On the other hand, the luxO disruption resulted in reduction of VVH production and expression of its gene vvhA. Expression of other two genes affecting the QS circuit, luxT and rpoN, were also significantly decreased. The regulation systems of VVP production were found to exert their action during the stationary phase of the bacterial growth and to be operated strongly at 26 °C. By contrast, those of VVH production apparently started at the log phase and were operated more effectively at 37 °C.
Keywords
Vibrio vulnificus
Metalloprotease
Hemolysin
Quorum sensing
Autoinducer
Note
This is an Accepted Manuscript of an article published by Springer
Published Date
2014-02
Publication Title
World Journal of Microbiology and Biotechnology
Volume
volume30
Issue
issue2
Publisher
Springer
Start Page
681
End Page
691
ISSN
09593993
NCID
AA10811107
Content Type
Journal Article
language
英語
OAI-PMH Set
岡山大学
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isVersionOf https://doi.org/10.1007/s11274-013-1501-3
Project
Collaborative Research of Okayama University for Infectious Diseases in India