Fig. 3: STM utilizes macrophage-derived 3PG as a major carbon source for intracellular replication and systemic infection.

a Replication of the wild-type (wt), pgtP mutant, or pgtP complemented STM strains in PMs. b Survival curves of mice infected i.p. with the wt (n = 16 mice), pgtP mutant (n = 14 mice), or pgtP complemented strains (n = 14 mice). c Liver and spleen bacterial burdens in mice infected with the wt, pgtP mutant, or pgtP complemented strains. d Replication of the wt or pgtP mutant STM strains in PMs cultured in RPMI medium containing 10 or 20 mM glucose. e Survival curves of mice infected i.p. with the wt or pgtP mutant STM strain and then injected i.p. with PBS or 20 mg of glucose every two days until 20 dpi or death (n = 8 mice per group). f Liver and spleen bacterial burdens in mice infected with the wt or pgtP mutant STM strain. Mice were infected as described in e. g Replication of wt STM in phgdh-overexpressing (OE:+) or control (OE:−) RAW264.7 cells in the presence or absence of 1 mM 3PG. h Replication of the wt, pgtP mutant, and ptsG manXYZ glk triple mutant STM strains in PMs. i Competitive index of the STM pgtP mutant versus the ptsG manXYZ glk triple mutant in the liver and spleen of infected mice. Data are presented as mean ± SD, n = 3 independent experiments a, d, g, h, n = 7 c, f or n = 9 i mice per group. P values were determined using two-tailed unpaired Student’s t test (a, g, h), log-rank Mantel–Cox test (b, e), Mann–Whitney U test (c, f, i) or one-way ANOVA (d). P = 0.0002 and 0.0012 for liver and spleen, respectively, based on raw CFU values of the pgtP mutant vs. ptsG manXYZ glk triple mutant (i). Source data are included in Source Data file.