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Acute lung injury (ALI) is considered as a severe respiratory disease with aggravated inflammatory responses. Krüppel-like factor 9 ( KLF9 ), a member of KLF family, has been reported to be involved in inflammatory disorders. However, the effect of  KLF9  in ALI has not been elucidated. Here the present study was to clarify the role of  KLF9  and its mechanism in ALI. The ALI  in vitro  model was established with lipopolysaccharide (LPS)-treated RAW264.7 cells. Mice were injected with LPS to conduct an ALI  in vivo  model. The expression of  KLF9  and gasdermin D ( GSDMD ) was examined using quantitative reverse transcription-PCR, haematoxylin-eosin/immunohistochemistry staining and western blot assays. Enzyme-linked immunosorbent assay was employed to detect the levels of inflammatory cytokines. JASPAR database was used to predict the recognition motif of  KLF9 , and the relationship between  KLF9  and  GSDMD  was determined by luciferase reporter assay and chromatin immunoprecipitation analysis. The number of neutrophils in bronchoalveolar lavage fluid as well as the wet/dry weight ratio was caculated. The results showed that The expression of  KLF9  in lung was significantly increased in LPS-stimulated mice. Moreover,  KLF9  knockout relieved the lung injury in ALI mice.  GSDMD  is one of targets genes of the transcription factor  KLF9 .  KLF9  knockout induced a decreased expression of  GSDMD  in LPS-treated mice. Furthermore, in RAW264.7 cells after LPS administration,  KLF9  knockdown reduced the levels of inflammatory factors and suppressed the expression of  GSDMD . In summarise, these findings exhibited that  KLF9  knockout could mitigate the lung injury and inflammatory responses in ALI mice by directly regulating  GSDMD .

Down-regulation of KLF9 ameliorates LPS-caused acute lung injury and inflammation in mice via reducing GSDMD expression