| First Author | An HS | Year | 2023 |
| Journal | Biochem Biophys Res Commun | Volume | 652 |
| Pages | 14-21 | PubMed ID | 36806084 |
| Mgi Jnum | J:334454 | Mgi Id | MGI:7441642 |
| Doi | 10.1016/j.bbrc.2023.02.029 | Citation | An HS, et al. (2023) Lipocalin-2 deletion attenuates lipopolysaccharide-induced acute lung inflammation via downregulating chemotaxis-related genes. Biochem Biophys Res Commun 652:14-21 |
| abstractText | Lipocalin-2 (LCN2) is an acute phase protein used as a biomarker for acute lung injury (ALI). Although the innate immune functions of LCN2 have been studied, how LCN2 contributes to ALI induced by lipopolysaccharide (LPS) remains unknown. In this study, we investigated the effect of LCN2 deletion on LPS-induced ALI using RNA-sequencing. LPS-treated LCN2 knockout (KO) mice had a decreased histopathological score and reduced neutrophil and macrophage infiltration in lung tissue compared with LPS-treated WT mice. RNA-sequencing analysis identified 38 differentially expressed genes (DEGs), including Cxcl5, Cxcl13, Xcl1, Saa1, and Cd14. In particular, Gene Ontology analysis of DEGs revealed a significant reduction in the inflammatory response, neutrophil chemotaxis, and chemokine-mediated signaling in LPS-treated LCN2KO mice compared with LPS-treated WT mice. Thus, these results suggest that LCN2 deletion alleviates LPS-induced ALI and that LCN2 may be involved in chemotaxis-related gene expression. |
