In the previous project researchers demonstrated that mislocalized CFTR is associated with an increase in intracellular Ca2+ content and this mechanism favoures the mithocondrial Ca2+ uptake, predisposing the organelle to a major stress responsivity . In this project they demonstrated that Pseudomonas aeruginosa affects mithocondrial Ca2+ signalling and physiology. The Pseudomonas protein Flagellin is an inducer of mithocondrial dysfunction favouring the Ca2+ increase in mithocondrial matrix. Finally, Ca2 + dependent disfunctioning mithocondria activate inflammosome response. An alternative strategy for treating exacerbated Pseudomonas aeruginosa-triggered inflammation in CF have to take in account the possibility to rescue mithocondrial physiology.