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Metalloprotease is not essential for Vibrio vulnificus virulence in mice
1Department of Microbiology and Immunology, College of Medicine, National Cheng-Kung University, Tainan 701, Taiwan.
Abstract:
Previous work suggested that a metalloprotease, Vvp, may be a virulence factor of Vibrio vulnificus, which causes severe wound infection and septicemia in humans. To determine the role of Vvp in pathogenesis, we isolated an isogenic protease-deficient (PD) mutant of Vibrio vulnificus by in vivo allelic exchange. This PD mutant was as virulent as its parental strain in mice infected intraperitoneally and was 10-fold more virulent in mice infected via the oral route. Furthermore, the PD mutant was indistinguishable from its parental strain in invasion from peritoneal cavity into blood stream, enhancement of vascular permeability, growth in murine blood, and utilization of hemoglobin and transferrin. These data suggest that Vvp is not essential for virulence in the mouse. However, the cytolysin activity in the culture supernatant of the PD mutant was found to be twofold higher than that of the wild-type strain and remained for a much longer period. The higher cytolysin activity of the PD mutant may be associated with the enhanced virulence in mice infected via the oral route.
Insights
The metalloprotease Vvp is not essential for Vibrio vulnificus virulence in mice. However, a protease-deficient mutant showed increased cytolysin activity and enhanced oral virulence, suggesting a role for cytolysin in pathogenesis.
Area of Science:
- Microbiology
- Pathogenesis Research
- Bacterial Virulence Factors
Background:
- Vibrio vulnificus causes severe human infections, including wound infections and septicemia.
- The metalloprotease Vvp was previously hypothesized to be a key virulence factor.
Purpose of the Study:
- To investigate the role of Vvp in the pathogenesis of Vibrio vulnificus.
- To determine if Vvp is essential for bacterial virulence in a murine model.
Main Methods:
- Isolation of an isogenic protease-deficient (PD) mutant of Vibrio vulnificus using in vivo allelic exchange.
- Comparative virulence studies in mice via intraperitoneal and oral routes.
- Assessment of bacterial invasion, vascular permeability, growth in blood, and nutrient utilization.
Main Results:
- The PD mutant exhibited similar virulence to the parental strain after intraperitoneal infection.
- Oral infection with the PD mutant resulted in 10-fold higher virulence compared to the wild-type strain.
- The PD mutant displayed twofold higher and prolonged cytolysin activity in culture supernatant.
Conclusions:
- Vvp is not essential for Vibrio vulnificus virulence in the mouse model.
- Elevated cytolysin activity in the PD mutant may contribute to enhanced virulence via the oral route.
- Further research is needed to elucidate the precise role of Vvp and cytolysin in Vibrio vulnificus pathogenesis.