Sodium butyrate attenuates bovine mammary epithelial cell injury by inhibiting the formation of neutrophil extracellular traps

中性粒细胞胞外陷阱 自噬 丁酸钠 PI3K/AKT/mTOR通路 化学 激酶 蛋白激酶B 蛋白激酶A 细胞外 安普克 丁酸盐 髓过氧化物酶 丁酸 细胞生物学 生物 生物化学 信号转导 细胞凋亡 炎症 免疫学 基因 发酵
作者
Yuhang Li,Juxiong Liu,Yueyao Cui,Yu Cao,Ping Xu,Xingchi Kan,Wenjin Guo,Shoupeng Fu
出处
期刊:International Immunopharmacology [Elsevier BV]
卷期号:110: 109009-109009 被引量:5
标识
DOI:10.1016/j.intimp.2022.109009
摘要

Neutrophil extracellular traps (NETs) are an important means by which the body fights against exogenous bacteria. However, studies have shown that excessive NETs release can damage other cells. Accumulating evidence has shown that butyric acid can alleviate the inflammatory response of cells. However, the effect of butyric acid on Staphylococcus aureus-induced NETs formation and its underlying mechanism are still unclear. In this study, western blotting, immunofluorescence and CCK-8 assays were used to examine the effect of NETs formation by sodium butyrate (NaB). The results showed that NaB suppressed the release of S. aureus-induced NETs formation, as indicated by decreases in the levels of DNA, histones, myeloperoxidase, and neutrophil elastase. S. aureus can induce autophagy, and autophagy plays a key role in the formation of NETs. Our data showed that NaB activated mammalian target of rapamycin (mTOR) and the kinases protein kinase B (AKT) and unc-51 like kinase 1 (ULK1) at Ser757 and inhibited AMP-activated protein kinase (AMPK). To explore whether NaB inhibited the formation of NETs by inhibiting autophagy, we added 3-methyladenine (autophagy inhibitor) (3-MA, 5 mM) to bovine neutrophils, and the results showed that 3-MA significantly inhibited NETs release. Furthermore, we found that NETs and their component histones exhibited significantly increased the cytotoxic effects on bovine mammary epithelial cells (BMECs), indicating that NETs and their component histones play a key role in BMEC damage. In conclusion, NaB can reduce the excessive formation of NETs by inhibiting autophagy, thus reducing the damaging effect of NETs on BMECs.
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