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. 2025 Jul 31;10(8):e00361-25. doi: 10.1128/msphere.00361-25

Fig 2.

Graphs depict NMN treatment in macrophage-depleted mice, showing no survival benefit, no reduction in cytokine levels, or bacterial burden. FK866 reduces fluorescence intensity and hvKP phagocytosis, but NMN co-treatment can counteract these effects.

The protective effect of NMN on the survival rate of hvKP BSI depends on macrophages. (A) Survival rate of hvKP BSI in macrophage-depleted mice with or without NMN treatment (n = 8) (1.0  ×  103 CFU). (B and C) Levels of IL-6, IL-1β, and TNF-α and bacterial load in the circulation and visceral organs in macrophage-depleted mouse liver with or without NMN treatment at 24 hpi (n = 6). (D) Phagocytic capacity of marrow-derived macrophages (BMDMs) from NMN (500 µM)- or FK866 (25 nM)-treated and vehicle controls using flow cytometry analysis at 1 hpi. (E and F) Gentamicin protection assay, intracellular bacterial counts of BMDMs from NMN (500 µM)- or FK866 (25 nM)-treated and vehicle controls at 1 and 4 hpi. Data are representative results from three independent experiments (mean  ±  SEM). *, P <  0.05; **, P <  0.01; ***, P <  0.001; ****, P < 0.0001; ns, not significant. NMN, β-nicotinamide mononucleotide; hvKP, hypervirulent Klebsiella pneumoniae; BMDM, bone marrow-derived macrophage; BSI, bloodstream infection; Clo-Lip, clodronate liposomes; CFU, colony-forming units; hpi, hours post-infection; MOI, multiplicity of infection; Control, no treatment or infection group; Vehicle, vehicle treatment and infection group.