The two aims of the project were to investigate if: i) Mitochondrial dysfunction in CF epithelial airways cells is direct link between Pseudomonas aeruginosa infection and inflammasome recruitment; ii) CFTR channel influences Ca2+ signalling and inter-organelle flux, compromising the mitochondrial quality control machinery. The project should obtain the following results: i) Characterization of roles of mitochondria and mitochondrial Ca2+ signaling in controlling activation of innate immune responses triggered by PAO; ii) Identification of new targets to design and test alternative pharmacological strategies to contrast the PAO-dependent innate immune response.