Pseudomonas aeruginosa Expresses a Lethal Virulence Determinant, the PA-I Lectin/Adhesin, in the Intestinal Tract of a Stressed Host

In Brief 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. The presence of Pseudomonas aeruginosa in the intestinal tract of a stressed host is associated with a high mortality rate in both humans and animals. Using a mouse model of lethal gut-derived sepsis due to this organism, the authors demonstrate that local factors within the intestinal tract of a stressed host enhance the virulence of this feared pathogen by activating elements within bacteria that dysregulate the intestinal epithelial barrier.