〔Abstract〕 Objective To study the biological function ofLamtor2 gene and its mechanism in the process ofLamtor2 infection, the model ofLamtor2 macrophage conditioned knockout mice infected with KP was established. Methods Lamtor2 flox /+mice were introduced for self-crossing, andLyz2-Cre mice were hybridized withLamtor2 flox /+to obtain offspring mice withLamtor2 flox / flox Lyz2-Cre-/-andLamtor2 flox /+Lyz2-Cre+/-. The two genotypes were hybridized to obtain control mice(Lamtor2 flox / flox Lyz2-Cre-/-) andlamtor2 conditional knockout mice(Lamtor2 flox / flox Lyz2-Cre+/-). The toe genomic DNA of mice was extracted and amplified by polymerase chain reaction(PCR). The genotypes of offspring mice were identified by agar-gel electrophoresis and alveolar macrophages were extracted. TheLamtor2 gene knockout effect was verified by RT-qPCR and Western blot. Mice were infected with Kp and their survival conditions were observed. The expression levels of TNF-α, IL-1β and Cxcl1 after Kp infection with alveolar macrophages were detected by qRT-PCRin vitro, and the comparison between the two groups was performed byttest. Western blot was used to verify the expression level of iNOS. Results Lamtor2 conditional gene knockout mouse model was successfully established withviableand fertile offspring. Compared with control mice, experimental mice had lower survival rate after Kp infection. The levels of TNF-α(t=17.54, 0.44±0.050,P=0.003 2), IL-1β(t=15.37, 0.35±0.043,P=0.004 2), and Cxcl1(t=37.82,0.23±0.043,P=0.000 7) fromLamtor2 flox / flox Lyz2-Cre+/-mouse alveolar macrophages reduced, and the iNOS expression decreased. Conclusion Lamtor2 knockout mice are constructed, and the survival rate of mice and iNOS expression of alveolar macrophges decreases after infected with Kp.