Zinc-dependent substrate-level phosphorylation powers Salmonella growth under nitrosative stress of the innate host response
Fig 5
Glycolysis enhances the recovery of Salmonella from nitrosative stress.
(A) Growth of wild-type (WT) and ΔpfkAB Salmonella in LB broth that was left untreated (ctrl) or treated with 500 μM DETA NONOate (dNO) (N = 5, mean). (B) Intracellular replication of WT and ΔpfkAB Salmonella 20 h after challenge of J774 macrophages. Select samples were treated with 500 μM of the iNOS inhibitor N6-(1-iminoethyl)-L-lysine (L-NIL) (N = 4–8, mean ± S.D.). ***, p < 0.001 as determined by two-way ANOVA. (C) Survival of C57BL/6 or iNOS deficient (iNOS-/-) mice after i.p. inoculation of 100 CFU of wild-type WT or ΔpfkAB Salmonella. (N = 9–10 mice). p < 0.01 for both C57BL/6 and iNOS-/-, as determined by logrank analysis. (D) Growth of the indicated Salmonella strains in EG minimal media. Where indicated, the specimens were treated with 750 μM spermine NONOate (+ sNO) (N = 4, mean ± S.E.M.). (E) Replication of Salmonella in J774 macrophages in the presence or absence of L-NIL (N = 4–8, mean ± S.D.). (F) Survival of C57BL/6 and iNOS-/- mice after i.p. challenge with 100 CFU of WT, ΔatpB, or Δnuo Δndh Salmonella. (N = 5 or 10 mice).