Pseudomonas aeruginosa expresses a lethal virulence determinant, the PA-I lectin/adhesin, in the intestinal tract of a stressed host: the role of epithelia cell contact and molecules of the Quorum Sensing Signaling System.

OBJECTIVE: We have previously demonstrated that P. aeruginosa can have profound effects on the intestinal epithelial barrier via one of its virulence factors, the PA-I lectin/adhesin. The aims of the present study were to further characterize the interaction of P. aeruginosa and the intestinal epithelium using both in vitro and in vivo approaches.
METHODS: In vitro assays examining the effect of bacterial growth phase, epithelial cell contact, and butanoyl homoserine lactone (C4-HSL), a quorum sensing signaling molecule know to affect various extracellular virulence factors in P. aeruginosa, on PA-I expression in P. aeruginosa were performed. In vivo studies were carried out by modeling catabolic stress in mice using a 30% surgical hepatectomy and direct introduction of P. aeruginosa and various virulence components into the cecum. The effect of this model on PA-I expression in P. aeruginosa was determined.
RESULTS: Results demonstrated that PA-I expression in P. aeruginosa is affected by its phase of growth, its contact to the intestinal epithelium, and its exposure to the quorum sensing molecule, C4-HSL. Furthermore, data from the present study suggest that the PA-I lectin/adhesin of P. aeruginosa may be increased in vivo by local factors within the cecum of mice in response to surgical stress.
CONCLUSIONS: These data indicate that multiple factors present in the intestinal microenvironment of a stressed host may induce certain opportunistic pathogens to express key virulence factors leading to a state of lethal gut-derived sepsis.