Mitochondrial Ca2+-dependent NLRP3 activation exacerbates the Pseudomonas aeruginosa-driven inflammatory response in cystic fibrosis.

作者: Alessandro Rimessi , Valentino Bezzerri , Simone Patergnani , Saverio Marchi , Giulio Cabrini

DOI: 10.1038/NCOMMS7201

关键词:

摘要: The common pathological manifestation of cystic fibrosis (CF) is associated with an excessive lung inflammatory response characterized by interleukin-1β accumulation. CF airway epithelial cells show exacerbated pro-inflammatory to Pseudomonas aeruginosa; however, it unclear whether this heightened intrinsic lacking transmembrane conductance regulator (CFTR). Here we demonstrate that the degree and quality in are supported P. aeruginosa-dependent mitochondrial perturbation, which flagellin inducer Ca(2+) uniporter (MCU) a signal-integrating organelle member for NLRP3 activation IL-1β IL-18 processing. Our work elucidates regulation inflammasome deepens our understanding significance mitochondria Ca(2+)-dependent control inflammation.

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