luxS and smcR Quorum-Sensing System of Vibrio vulnificus as an Important Factor for In Vivo Survival

  • SHIN NA-RI (Department of Infectious Diseases, College of Veterinary Medicine and School of Agricultural Biotechnology, Seoul National University) ;
  • BAEK CHANG-HO (Department of Life Science, College of Natural Science, Sogang University) ;
  • LEE DEOG-YONG (Department of Infectious Diseases, College of Veterinary Medicine and School of Agricultural Biotechnology, Seoul National University) ;
  • CHO YOUNG-WOOK (Department of Infectious Diseases, College of Veterinary Medicine and School of Agricultural Biotechnology, Seoul National University) ;
  • PARK DAE-KYUN (Department of Life Science, College of Natural Science, Sogang University) ;
  • LEE KO-EUN (Department of Life Science, College of Natural Science, Sogang University) ;
  • KIM KUN-SOO (Department of Life Science, College of Natural Science, Sogang University) ;
  • YOO HAN-SANG (Department of Infectious Diseases, College of Veterinary Medicine and School of Agricultural Biotechnology, Seoul National University)
  • Published : 2005.12.01

Abstract

Vibrio vulnificus is an opportunistic pathogen that causes a septicemia and expresses numerous virulence factors, in which luxS and smcR are genes encoding for components responsible for quorum-sensing regulation. In the present study, null mutants were constructed with lesions in each or both of these two genes from the V. vulnificus Vv$\Delta$Z strain, which is a lacZ$^{-}$ and chloramphenicol/streptomycin-resistant derivative of the wild-type ATCC29307 strain, and their phenotypes related to virulence were compared with those of the parental cells. $LD_{50}$ and histopathological findings of luxS-, smcR-, or luxS- smcR- deficient mutant were not different from those of the parent strain, a lacZ-deficient streptomycin-resistant strain in mice. However, time of death in mice was delayed, and numbers of bacteria survived in bloodstream after intraperitoneal injection in mice were decreased by mutation, especially luxS and smcR double mutant (VvSR$\Delta$ZSR). These phenomena were supported by increased serum sensitivity and delayed bacterial proliferation in both murine blood and iron-restricted medium. These results suggest that the luxS and luxR homologous genes in V. vulnificus could playa role in bacterial survival in host by enhancing proliferation and adjusting to changed environment.

Keywords

References

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