Figure 5: Proposed role of Lpf in EHEC pathogenicity.
The figure summarizes the main results obtained from this study. The survival rate of EHEC is shown in red. In the gastric compartment EHEC can survive; while in the small intestinal compartments, mortality is followed by a bacterial growth at the end of digestion, in the large intestine, the pathogenic bacteria are not able to maintain and are progressively eliminated. The lpfAOI-141 and lpfAOI-154gene expression profiles, analyzed throughout the simulated human digestive tract, are shown in blue and green respectively. lpf expression is increased during bacterial transit through the gastric and small intestine, mainly in the terminal ileum. Gastric pH and bile salts concentration in small intestine are hypothesized to be the factors inducing lpf expression. The absence of Lpf impairs EHEC ability to interact with ileal Peyer’s patches. Our results suggest that EHEC might colonize the terminal ileum at the early stages of infection in humans, and that Lpf are involved in the interactions of EHEC with ileal Peyer’s patches and are needed for an active translocation of the pathogen across M-cells.
