Overexpression of IFIT1 protects against LPS-induced acute lung injury via regulating CCL5-p65NF-?B signaling

被引：7
作者：
Jiang, Wei [1 ,2 ]
Zhang, Yafei [2 ]
Sheng, Yingying [1 ,2 ]
Liu, Min [1 ,2 ]
Du, Changlin [1 ]
Pan, Xueyin [2 ]
Huang, Cheng [2 ]
Li, Jun [2 ]
Wang, Yuanyuan [1 ,2 ]
机构：
[1] Anhui Med Univ, Anhui Inst Innovat Drugs, Sch Pharm, Inflammat & Immune Mediated Dis Lab Anhui Prov, Hefei 230032, Anhui, Peoples R China
[2] Anhui Med Univ, Affiliated Hosp 2, Dept Pharm, Hefei 230601, Anhui, Peoples R China
来源：
INTERNATIONAL IMMUNOPHARMACOLOGY | 2023年 / 114卷
关键词：
IFIT1; Acute lung injury; Inflammation; Apoptosis; CCL5 NF-kB signal pathway; INFLAMMATION; EXPRESSION;
D O I：
10.1016/j.intimp.2022.109485
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
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-alpha, IL-1 beta 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 C-C motif chemokine ligand 5 (CCL5) partially eliminated the protective effects of IFIT1 and promoted the expression of inflammatory cytokines TNF-alpha, IL-1 beta and IL-6 by CCL5-p65NF-kappa B signaling pathway. This study demonstrated that IFIT1 attenuated ALI-associated inflammation and cell apoptosis by regulating the CCL5-p65NF-kappa B signaling pathway. These findings are of great significance for the treatment of lung injury.
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页数：13
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