β-Nicotinamide mononucleotide protects against hypervirulent Klebsiella pneumoniae bloodstream infection and liver injury.

Cao Z, Meng B, Chen J, Ge R, Liu Y, Li J

mSphere31 Jul 2025Cited by 3 (Europe PMC)

PMID40742124PMCIDPMC12379607DOI10.1128/msphere.00361-25PepBankPUB-40742124

Summary

In clinical practice, hypervirulent Klebsiella pneumoniae (hvKP) often causes bloodstream infections (BSI) and liver abscesses; however, the mechanism of hvKP-induced liver abscess formation remains unclear. β-Nicotinamide mononucleotide (NMN) has been reported to have potential therapeutic effects on sepsis, but its impact on hvKP BSI is still unclear. Supplementation with NMN improved the survival rate of hvKP BSI, and the protective effects of NMN disappeared after macrophage depletion. NMN treatment can reduce NF-κB signaling pathway activation in bone marrow-derived macrophages (BMDM) after hvKP infection, as well as the transcription of Il6, Il1b, Tnf, and Cxcl2. NMN, combined with antibiotic therapy, blocked the formation of hvKP liver abscesses. The treatment regimen of NMN combined with antibiotics effectively reduced the levels of inflammatory factors in the liver, inhibited the activation of the NF-κB signaling pathway, and reduced the infiltration of neutrophils into the liver. These results indicate that NMN exerts a protective effect against hvKP BSI by inhibiting excessive inflammatory response, and NMN has therapeutic potential for preventing liver injury caused by hvKP.IMPORTANCEThis study found that β-nicotinamide mononucleotide (NMN) can protect mice against hvKP BSI via inhibiting the NF-κB signaling pathway activation. Supplementing NMN with antibiotic treatment alleviated the inflammatory response of the liver and reduced the formation of liver abscess, providing insight into the mechanism of liver abscess research.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study11

7 results from studies that gave the peptide. No result from this study comes from people.

01AnimalAnimal study (in vivo)Efficacy outcome
In mice with hvKP bloodstream infection, NMN improved survival.
In plain wordsIn mice with hvKP bloodstream infection, NMN increased survival.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseSurvival
Study
mousen: not reported in source
hypervirulent Klebsiella pneumoniae bloodstream infection
Outcome group
Mortality · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
Supplementation with NMN improved the survival rate of hvKP BSI, and the protective effects of NMN disappeared after macrophage depletion.
1 context sentence(design, population, supporting numbers)
Summary · context
IMPORTANCEThis study found that β-nicotinamide mononucleotide (NMN) can protect mice against hvKP BSI via inhibiting the NF-κB signaling pathway activation.
Show in the study text Report a problemFND-4074212401
02AnimalAnimal study (in vivo)Mechanism
In mice with hvKP bloodstream infection, NMN lost its protective effect after macrophage depletion.
In plain wordsIn mice with hvKP bloodstream infection, NMN no longer protected the mice after macrophage removal.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
No significant changeProtection after macrophage depletion
Study
mousen: not reported in source
hypervirulent Klebsiella pneumoniae bloodstream infection
Outcome group
Immune response · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
Supplementation with NMN improved the survival rate of hvKP BSI, and the protective effects of NMN disappeared after macrophage depletion.
Show in the study text Report a problemFND-4074212402
03LabIn vitro (cells)Mechanism
In hvKP-infected bone marrow-derived macrophages, NMN reduced NF-κB signaling activation.
In plain wordsIn cells infected with hvKP, NMN reduced NF-κB signaling in bone marrow-derived macrophages.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseMacrophage NF-kappaB signaling
Study
n: not reported in source
hvKP-infected bone marrow-derived macrophages
Outcome group
Receptor activity and mechanism · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
NMN treatment can reduce NF-κB signaling pathway activation in bone marrow-derived macrophages (BMDM) after hvKP infection, as well as the transcription of Il6, Il1b, Tnf, and Cxcl2.
Show in the study text Report a problemFND-4074212403
04LabIn vitro (cells)Mechanism
In hvKP-infected bone marrow-derived macrophages, NMN reduced Il6 transcription.
In plain wordsIn cells infected with hvKP, NMN reduced Il6 gene activity in bone marrow-derived macrophages.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseIl6 transcription
Study
n: not reported in source
hvKP-infected bone marrow-derived macrophages
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
NMN treatment can reduce NF-κB signaling pathway activation in bone marrow-derived macrophages (BMDM) after hvKP infection, as well as the transcription of Il6, Il1b, Tnf, and Cxcl2.
Show in the study text Report a problemFND-4074212404
05LabIn vitro (cells)Mechanism
In hvKP-infected bone marrow-derived macrophages, NMN reduced Il1b transcription.
In plain wordsIn cells infected with hvKP, NMN reduced Il1b gene activity in bone marrow-derived macrophages.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseIl1b transcription
Study
n: not reported in source
hvKP-infected bone marrow-derived macrophages
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
NMN treatment can reduce NF-κB signaling pathway activation in bone marrow-derived macrophages (BMDM) after hvKP infection, as well as the transcription of Il6, Il1b, Tnf, and Cxcl2.
Show in the study text Report a problemFND-4074212405
06LabIn vitro (cells)Mechanism
In hvKP-infected bone marrow-derived macrophages, NMN reduced Tnf transcription.
In plain wordsIn cells infected with hvKP, NMN reduced Tnf gene activity in bone marrow-derived macrophages.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseTnf transcription
Study
n: not reported in source
hvKP-infected bone marrow-derived macrophages
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
NMN treatment can reduce NF-κB signaling pathway activation in bone marrow-derived macrophages (BMDM) after hvKP infection, as well as the transcription of Il6, Il1b, Tnf, and Cxcl2.
Show in the study text Report a problemFND-4074212406
07LabIn vitro (cells)Mechanism
In hvKP-infected bone marrow-derived macrophages, NMN reduced Cxcl2 transcription.
In plain wordsIn cells infected with hvKP, NMN reduced Cxcl2 gene activity in bone marrow-derived macrophages.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseCxcl2 transcription
Study
n: not reported in source
hvKP-infected bone marrow-derived macrophages
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
NMN treatment can reduce NF-κB signaling pathway activation in bone marrow-derived macrophages (BMDM) after hvKP infection, as well as the transcription of Il6, Il1b, Tnf, and Cxcl2.
Show in the study text Report a problemFND-4074212407

Studies that did not test the peptide alone4

In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking NMN (nicotinamide mononucleotide).

08AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Efficacy outcome
In mice with hvKP infection, NMN combined with antibiotics blocked liver abscess formation.
In plain wordsIn mice with hvKP infection, NMN with antibiotics prevented liver abscess formation.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseLiver abscess formation
Study
mousen: not reported in source
hypervirulent Klebsiella pneumoniae bloodstream infection
Outcome group
Infection and antimicrobial activity · Liver
Source sentences
Summary
NMN, combined with antibiotic therapy, blocked the formation of hvKP liver abscesses.
In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).
Show in the study text Report a problemFND-4074212408
09AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Efficacy outcome
In mice with hvKP infection, NMN combined with antibiotics reduced liver inflammatory factor levels.
In plain wordsIn mice with hvKP infection, NMN with antibiotics reduced inflammatory substances in the liver.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseLiver inflammatory factors
Study
mousen: not reported in source
hypervirulent Klebsiella pneumoniae bloodstream infection
Outcome group
Inflammation markers · Liver
Source sentences
Summary
The treatment regimen of NMN combined with antibiotics effectively reduced the levels of inflammatory factors in the liver, inhibited the activation of the NF-κB signaling pathway, and reduced the infiltration of neutrophils into the liver.
In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).
Show in the study text Report a problemFND-4074212409
10AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Mechanism
In mice with hvKP infection, NMN combined with antibiotics inhibited liver NF-κB signaling activation.
In plain wordsIn mice with hvKP infection, NMN with antibiotics reduced NF-κB signaling in the liver.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseLiver NF-kappaB signaling
Study
mousen: not reported in source
hypervirulent Klebsiella pneumoniae bloodstream infection
Outcome group
Receptor activity and mechanism · Liver
Source sentences
Summary
The treatment regimen of NMN combined with antibiotics effectively reduced the levels of inflammatory factors in the liver, inhibited the activation of the NF-κB signaling pathway, and reduced the infiltration of neutrophils into the liver.
In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).
Show in the study text Report a problemFND-4074212410
11AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Efficacy outcome
In mice with hvKP infection, NMN combined with antibiotics reduced neutrophil infiltration into the liver.
In plain wordsIn mice with hvKP infection, NMN with antibiotics reduced neutrophil entry into the liver.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseLiver neutrophil infiltration
Study
mousen: not reported in source
hypervirulent Klebsiella pneumoniae bloodstream infection
Outcome group
Immune response · Liver
Source sentences
Summary
The treatment regimen of NMN combined with antibiotics effectively reduced the levels of inflammatory factors in the liver, inhibited the activation of the NF-κB signaling pathway, and reduced the infiltration of neutrophils into the liver.
In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).
Show in the study text Report a problemFND-4074212411

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
21 Oct 2026, 15:58 UTC
Study results updated
Version 1
21 Oct 2026, 12:50 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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