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Pseudomonas aeruginosa  can acquire and metabolize a variety of molecules including choline, an abundant host-derived molecule. In  P. aeruginosa , choline is oxidized to glycine betaine which can be used as an osmoprotectant, a sole source of carbon and nitrogen, and as an inducer of the virulence factor, hemolytic phospholipase C (PlcH) via the transcriptional regulator GbdR. The primary objective was to determine the contribution of choline conversion to glycine betaine to  P. aeruginosa  survival during mouse lung infection. A secondary objective was to gain insight into the relative contributions of the different roles of glycine betaine to  P. aeruginosa  survival during infection. Using a model of acute murine pneumonia, we determined that deletion of the choline oxidase system (encoded by  betBA ) decreased  P. aeruginosa  survival in the mouse lung. Deletion of the glycine betaine demethylase genes ( gbcA-B ), required for glycine betaine catabolism, did not impact  P. aeruginosa  survival in the lung. Thus, the defect of the  betBA  mutant was not due to a requirement for glycine betaine catabolism or dependence on a downstream metabolite. Deletion of  betBA  decreased the abundance of  plcH  transcript during infection, which suggested a role for PlcH in the  betBA  survival defect. To test the contribution of  plcH  to the  betBA  mutant phenotype a  betBAplcHR  double deletion mutant was generated. The  betBA  and  betBAplcHR  double mutant had a small but significant survival defect compared to the  plcHR  single mutant, suggesting that regulation of  plcH  expression is not the only role for glycine betaine during infection. The conclusion was that choline acquisition and its oxidation to glycine betaine contribute to  P. aeruginosa  survival in the mouse lung. While defective  plcH  induction can explain a portion of the  betBA  mutant phenotype, the exact mechanisms driving the  betBA  mutant survival defect remain unknown.

Choline Catabolism to Glycine Betaine Contributes to Pseudomonas aeruginosa Survival during Murine Lung Infection