P. aeruginosa is able to infect hosts by using a broad panel of virulence factors. One of the most important is the type III secretion system (T3SS), a syringe-like appendix that allows the injection of 4 exotoxins (ExoS, ExoT, ExoU and ExoY) directly into the cytoplasm of target cells. Each T3SS effector is inactive when injected and requires a host cell cofactor to be activated and acquire its enzymatic activity.
ExoY’s nucleotidyl cyclase activity is activated by binding to eukaryotic F-actin, and induces the accumulation of cyclic nucleotide monophosphates (cNMPs) in host cell, thus disrupting numerous signaling pathways.
Unlike other T3SS toxins known to contribute directly to cell death, the role of ExoY in P. aeruginosa virulence has not yet been clearly elucidated.
We aim is to identify the molecular pathways modulated by ExoY in infected airway epithelial cells.
