Vibrio vulnificusmetalloprotease VvpE is essentially required for swarming

Abstract

Bacterial swarming constitutes a good in vitro model for surface adherence and colonization, and is accompanied by expressions of virulence factors related to invasiveness. In this study, it was determined that Vibrio vulnificus swarming was abolished by mutation of the vvpE gene encoding a metalloprotease VvpE and this swarming defect was recovered by complementation of the vvpE gene. Expression of the vvpE gene began simultaneously with the beginning of swarming and increased along with expression of the luxS gene encoding the synthase of the precursor of quorum-sensing signal molecule autoinducer 2, and this increased vvpE expression was decreased by mutation of the luxS gene. Moreover, VvpE destroyed IgA and lactoferrins, which are responsible for mucosal immunity. These results suggest that VvpE may play important roles in the surface adherence and colonization of V. vulnificus by facilitating swarming and in the mucosal invasion of V. vulnificus by destroying IgA and lactoferrin.

The importance of the Rcs phosphorelay in the survival and pathogenesis of the enteropathogenic yersiniae

“…Metalloproteases have a variety of putative roles, and thus the significance of this high-level expression can only be hypothesized. Metalloprotease expression has previously been shown to affect surface adherence and colonization by Vibrio vulnificus due to an effect on swarming behaviour (Kim et al, 2007); however, metalloproteases may also be involved in mammalian tissue toxicity (Bowen et al, 2003) and may be important in disease pathology. The putative intimin is likely to act as an adhesin in the gut whilst the putative ShET2-like enterotoxin (YPO1002) is likely to play a role in the pathology of Y. pseudotuberculosis infection by altering the permeability of the epithelial cells of the intestinal wall and causing diarrhoea.…”

Role of GacA in virulence of Vibrio vulnificus

“…The concentric rings of V. vulnificus on low-viscosity agar are more likely related to stationary phase responses to nutrient limitation or perhaps to biofilm formation that occurs at the air-liquid interface. V. vulnificus vvpE mutants described elsewhere are also defective in ring formation (Kim et al, 2007), and since gacA mutants show reduced protease activity and vvpE transcript levels, these defects may also contribute to the differential growth on motility agar.…”

Change ofVibrio vulnificusMetalloprotease VvpE Production by Temperature and Salinity

“…In addition, the AI-2 bioassay is known to be too vulnerable to accurately measure the activity of AI-2-QSS (24). Similarly, the luxS expression level alone may not represent actual AI-2-QSS activity because AI-2 production is mediated by several spontaneous non-enzymatic reactions, as well as the enzymatic action of LuxS (10 In V. vulnificus, AI-2 production is mediated by the enzymatic action of LuxS (13,18), and AI-2 signaling is transferred to the master regulator SmcR (a LuxR homolog) via LuxO and LuxT (25). It has been well documented that vvpE transcription is positively or negatively regulated by luxS, luxO, or smcR mutations, respectively (6,13).…”

“…The PCR product was then subcloned into pQF52 (15). From the resulting plasmid pRC130, the BamHI-ScaI fragment containing the P luxS ::lacZ fragment was isolated and subcloned into pDM4 (18). The resulting plasmid pRC136 was transformed into E. coli SY327 λpir and SM10 λpir (14), and transferred to CMM2101 by conjugation.…”