Back

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.

2025-08-07 microbiology
10.1101/2025.08.07.669126 bioRxiv
Show abstract

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.

Matching journals

The top 3 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.