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

Fig 4.

Liver morphology, histology, bacterial burden, and serum markers indicate hvKP causes liver damage and inflammation, while Clo-Lip, NMN, and AT reduce necrosis, inflammatory infiltration, ALT, AST, and LDH without reducing CFU counts.

Supplementation of NMN combined with antibiotic treatment to alleviate liver injury and abscess caused by hvKP. (A through D) Liver, bacterial load, ALT levels, and HE staining of liver tissue in mice infected with 1.0 × 103 CFU of ATCC 43816 at 18 hpi with or without clodronate liposome treatment (n = 6). (E) NMN (500 mg/kg, i.p.) was supplemented 1 h before infection and gentamicin (50 mg/kg, i.p.) was administered at 4.5 hpi, and mice were euthanized at 24 hpi. Mouse liver right upper lobes in different groups (n = 6). (F) Bacterial load of liver tissue in different groups (n = 6). (G–I) ALT, AST, and LDH levels in different groups (n = 6). 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; ALT, alanine aminotransferase; AST, aspartate aminotransferase; LDH, lactate dehydrogenase; AT, antibiotic treatment after hvKP infection; CFU, colony-forming units; hpi, hours post-infection. Control, no treatment or infection group; Vehicle, vehicle treatment and infection group.