细胞外
活性氧
NADPH氧化酶
糖酵解
生物
烟酰胺腺嘌呤二核苷酸磷酸
先天免疫系统
免疫系统
毒素
细胞生物学
化学
微生物学
生物化学
分子生物学
氧化酶试验
新陈代谢
酶
免疫学
作者
Wei Liu,Di Wu,Shuangqiu Li,Jingnan Xu,Peixuan Li,Aimin Jiang,Yong Zhang,Ziyi Liu,Liqiang Jiang,Xinxin Gao,Zhengtao Yang,Zhengkai Wei
标识
DOI:10.1021/acs.jafc.1c05371
摘要
T-2 toxin (T-2) is a kind of trichothecene toxin produced from Fusarium fungi, which is an environmental pollutant that endangers poultry and human health. Heterophil extracellular traps (HETs) are not only a form of chicken immune defense against pathogen infection but also involved in pathophysiological mechanisms of several diseases. However, the immunotoxicity of T-2 on HET formation in vitro has not yet been reported. In this study, heterophils were exposed to T-2 at doses of 20, 40, and 80 ng/mL for 90 min. Observation of the structure of HETs by immunofluorescence staining and the mechanism of HET formation was analyzed by inhibitors and PicoGreen. These results showed that T-2-triggered HET formation consisted of DNA, elastase, and citH3. Furthermore, T-2 increased reactive oxygen species (ROS) generation, and the formation of T-2-triggered HETs was also decreased by the inhibitors of glycolysis, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, p38 and extracellular signal-regulated kinase (ERK)1/2 signaling pathways, suggesting that T-2-induced HETs are associated with glycolysis, ROS production, ERK1/2 and p38 signaling pathways, and NADPH oxidase. Taken together, this study elucidates the mechanism of T-2-triggered HET formation, and it may provide new insight into understanding the immunotoxicity of T-2 to early innate immunity in chickens.
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