趋化因子
CCL5
肿瘤坏死因子α
细胞凋亡
癌症研究
炎症
免疫学
信号转导
细胞生物学
生物
医学
T细胞
免疫系统
生物化学
白细胞介素2受体
作者
Wei Jiang,Yafei Zhang,Yingying Sheng,Min Liu,Changlin Du,Xue‐Yin Pan,Cheng Huang,Jun Li,Yuan‐Yuan Wang
标识
DOI:10.1016/j.intimp.2022.109485
摘要
Acute lung injury (ALI) is featured by intensive inflammatory responses causing significant morbidity and mortality. Interferon-induced protein with tetratricopeptide repeats 1 (IFIT1), induced by interferon (IFN), has been discovered to modulate viral infection and cell apoptosis and inhibit the production of pro-inflammatory cytokines. However, it’s role and mechanism in ALI remain unclear and need to be explored furtherly. Here, we discovered that IFIT1 decreased the expression of TNF-α, IL-1β and IL-6 in mouse-derived macrophage cells (MH-S) and alleviated apoptosis of murine lung epithelial cells (MLE-12) induced by MH-S cell supernatant, contributing to anti-inflammatory and antiapoptotic effects in vitro and in vivo. Moreover, RNA sequencing analysis (RNA-seq) showed that inflammatory chemokine CC motif chemokine ligand 5 (CCL5) partially eliminated the protective effects of IFIT1 and promoted the expression of inflammatory cytokines TNF-α, IL-1β and IL-6 by CCL5-p65NF-κB signaling pathway. This study demonstrated that IFIT1 attenuated ALI-associated inflammation and cell apoptosis by regulating the CCL5-p65NF-κB signaling pathway. These findings are of great significance for the treatment of lung injury.
科研通智能强力驱动
Strongly Powered by AbleSci AI