Vibrio vulnificus causes fatal septicemia in human hosts, which is the consequence of raw shellfish consumption. The mortality following septicemia is dependent on the in vivo production of inflammatory mediators, including tumor necrosis factor-alpha (TNFα). The present study was set up to investigate the association of quorum sensing in V. vulnificus with the host immune response. The effect of quorum sensing on cytotoxicity and the production of proinflammatory mediators was examined using the murine macrophage cell-line RAW264.7. Cytotoxicity was determined by measuring lactate dehydrogenase release in the culture medium. Extracellular products from luxS- and smcR-deficient mutants exhibited weak cytotoxic effects on RAW264.7 cells. The production of the proinflammatory cytokines TNFα, IL-1β and IL-6 was measured with real-time PCR and ELISA, and production was measured with Griess reagents. Mutation of both luxS and smcR delayed the transcription of TNFα, IL-1β and IL-6 genes. Also, levels of both TNFα and nitric oxide induced by luxS- and smcR-deficient mutants were significantly lower than those induced by parent strains. These results suggest that quorum sensing could be involved in the modulation of TNFα and nitric oxide produced from host cells by regulating virulence factors, and that V. vulnificus facilitates its host's mortality and bacterial survival by enhancing virulence on host cells.
Bibliographical noteFunding Information:
This study was supported by KOSEF and Brain Korea 21.
All Science Journal Classification (ASJC) codes
- Immunology and Allergy
- Microbiology (medical)
- Infectious Diseases