Salmonella Typhimurium impairs glycolysis-mediated acidification of phagosomes to evade macrophage defense
Fig 3
Macrophage depend on glycolysis for the clearance of intracellular bacteria.
(A) Bacterial burden expressed as colony forming units (CFU) after 24h of S. Typhimurium infection in 2-DG-treated WT BMDMs compared to untreated (UT) controls (n = 5). (B) Intracellular S. Typhimurium load in WT and IRΔmyel BMDMs after 24h of infection (n = 3). (C) S. Typhimurium in 4-OHT-treated WT BMDMs compared to untreated (UT) controls after 24h of infection (n = 3). (D) L. monocytogenes (E) S. aureus burden in 2-DG-treated WT BMDMs compared to untreated (UT) controls (n = 3). (F) S. aureus burden in WT and IRΔmyel BMDMs (n = 3) 24h post-infection. (G) Bacterial load in livers of WT and IRΔmyel mice after 3 days post S. Typhimurium infection or (H) 4-OHT-treated mice. Data represent 2 experiments with 5 mice each. Data are shown as mean ± S.E.M. and statistical significance calculated using student t-test and represented as * = p<0.05; ** = p<0.01; *** = p<0.001. (I) MFI of OVA323-339-MHC II complexes on the surface of WT BMDMs pre-treated with 2-DG and LPS (n = 3). (J) MFI of unprocessed Alexa647-labelled OVA in phagosomes isolated from 2-DG-treated BMDMs analyzed by flow cytometry (n = 3). All samples were pre-stimulated with LPS. (K) MFI of unprocessed Alexa647-labelled OVA in bead containing phagosomes isolated from S. Typhimurium-infected BMDMs analyzed by flow cytometry (n = 3).