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Vibrio vulnificus is an opportunistic pathogen thatcauses a septicemia and expresses numerous virulence factors,in which luxS and smcR are genes encoding for componentsresponsible for quorum-sensing regulation. In the presentstudy, null mutants were constructed with lesions in each orboth of these two genes from the V. vulnificus Vv.Z strain,which is a lacZ- and chloramphenicol/streptomycin-resistantderivative of the wild-type ATCC29307 strain, and theirphenotypes related to virulence were compared with those ofthe parental cells. LD50 and histopathological findings of luxS-,smcR-, or luxS- smcR- deficient mutant were not differentfrom those of the parent strain, a lacZ-deficient streptomycinresistantstrain in mice. However, time of death in mice wasdelayed, and numbers of bacteria survived in bloodstream afterintraperitoneal injection in mice were decreased by mutation,especially luxS and smcR double mutant (VvSR.ZSR). Thesephenomena were supported by increased serum sensitivityand delayed bacterial proliferation in both murine blood andiron-restricted medium. These results suggest that the luxSand luxR homologous genes in V. vulnificus could play a rolein bacterial survival in host by enhancing proliferation andadjusting to changed environment.

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