Monday, August 12, 2013
Pavilion (Sheraton San Diego)
Quorum sensing is a cell-cell communication system known to control many bacterial processes. In the present study, the functions of quorum sensing in the pathogenesis of Vibrio vulnificus, a foodborne pathogen, were assessed by evaluating the virulence of a mutant with disruption of the smcR gene encoding a LuxR homologue. When biofilm cells were used as an inoculum, the smcR mutant was impaired in virulence and colonization capacity in the infection of mice. The disruption of smcR also resulted in a decrease in histopathological damage in mouse jejunum tissue. These results indicated that SmcR is essential for V. vulnificus pathogenesis. Moreover, the smcR mutant exhibited significantly reduced biofilm detachment. Upon exposure to INT-407 host cells, the wild type, but not the smcR mutant, revealed accelerated biofilm detachment. The INT-407 cells elevated the expression of smcR, indicating that the accelerated biofilm detachment by the host cells is attributed to the increased cellular level of SmcR. Whole genome microarray analysis revealed that the genes primarily involved in biofilm detachment and formation are up- and down-regulated by SmcR, respectively. Among the SmcR-regulated genes, vvpE encoding an elastolytic protease was the most up-regulated and the purified VvpE appeared to stimulate the detachment of the preformed biofilm in a concentration-dependent manner. Consequently, the results suggest that the quorum sensing regulator SmcR enhances detachment of the V. vulnificus biofilms entering the host intestine and thereby promotes dispersal of the pathogen to new colonization sites, which is crucial for pathogenesis.