〔Abstract〕 Objective To establish the liver conditional knockout mouse model ofNod2gene infected byKlebsiella pneumoniae(K.pneumoniae),and to explore the role and mechanism ofNod2gene in the process of liver abscess caused byK.pneumoniaeinfections. Methods Nod2flox/floxmice were obtained by self-crossing ofNod2flox/+mice, andAlb-Cre+mice were hybridized withNod2flox/+to obtainNod2flox/+;Alb-Cre+mice, then the above two genotypes mice were crossed to obtain liver conditional knockout mice ofNod2gene(Nod2flox/flox;Alb-Cre+) and negative control mice in the same litter(Nod2flox/flox).The genomic DNA of mice toe was extracted and amplified by polymerase chain reaction(PCR).The genotypes of offspring were identified by agar-gel electrophoresis and the livers of mice were extracted.Real-time fluorescence quantitative PCR(RT-qPCR) and Western blot were used to verify the knockout efficiency ofNod2gene in the liver.Both experimental group and control group mice were infected withK.pneumoniae,and the survival rate and pathological changes of livers were observed at different time points, and mRNA expression levels of Tumor necrosis factor α(TNF-α),interleukin 1β(IL-1β) and C-X-C motif chemokine ligand 1(CXCL1) in the livers of experimental group and control group were detected by RT-qPCR 24 h postK.pneumoniaeinfections. Results The expression of NOD2 mRNA in the liver ofNod2flox/flox;Alb-Cre+mice decreased, and the Western blot results showed that the expression of NOD2 protein decreased.Compared with the control group, the survival rate of mice infected withK.pneumoniaein the experimental group decreased(median survival time=60.5 h,P=0.046 9) and the liver tissue showed more serious pathological damage, furthermore the mRNA expression levels of TNF-α,IL-1β and CXCL1 in the livers of experimental group were lower than those of the control group, and the difference was statistically significant(P<0.05). Conclusion NOD2 plays a protective role in the process of liver abscess induced byK.pneumoniaeinfections.