脂质运载蛋白
脂多糖
趋化因子
CD14型
趋化性
炎症
先天免疫系统
免疫学
CXCL5型
基因
生物
分子生物学
免疫系统
受体
内分泌学
遗传学
作者
Hyeong Seok An,Jaewoong Lee,So Jeong Lee,Eun Ae Jeong,Hyun Joo Shin,Kyung Eun Kim,Gu Seob Roh
标识
DOI:10.1016/j.bbrc.2023.02.029
摘要
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.
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