Sequestration of the phagocyte metabolite itaconate by P. aeruginosa RpoN promotes successful pulmonary infection
Beg, A. Z.; Liu, Z.; Chen, Y. T.; Talat, A.; Gowdy, G.; Miller, J. W.; Florek, L.; Dietrich, L.; Wang, C.; Lewis, I.; Wong, T. F. L.; Riquelme, S.; Prince, A. S.
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AbstractThe phagocyte immunometabolite itaconate, normally toxic to bacteria, functions as a signal to stimulate the adaptation of the pulmonary pathogen Pseudomonas aeruginosa to the lung. Itaconate is actively transported into P. aeruginosa where it induces {sigma}54 rpoN expression and co-valently binds cysteine residues on RpoN. RpoN not only functions as a sink to limit itaconate toxicity but S- itaconated RpoN promotes increased utilization of the Entner Doudoroff pathway, optimizing bacterial metabolism in the setting of inflammation. S-itaconation of RpoN directs a global metabolic response that fuels pulmonary infection.
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