Frontiers in Cellular and Infection Microbiology | |
Aflatoxin B1 Induces Reactive Oxygen Species-Mediated Autophagy and Extracellular Trap Formation in Macrophages | |
Jiang, Mingguo1  Yu, Lu2  Tang, Xudong3  An, Yanan4  Wang, Yang4  Zhang, Qiaoli4  Shi, Xiaochen4  Wang, Chao4  Shen, Fengge4  Liu, Mingyuan4  | |
[1] Guangxi Colleges and Universities Key Laboratory of Utilization of Microbial and Botanical Resources, Guangxi University for Nationalities, Nanning, China;Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, China;Key Lab for New Drug Research of TCM, Research Institute of Tsinghua University in Shenzhen, Shenzhen, China;Key Laboratory for Zoonosis Research, Ministry of Education, Institute of Zoonosis, First Hospital of Jilin University, College of Veterinary Medicine and College of Animal Science, Jilin University, Changchun, China | |
关键词: Aflatoxin B1; Reactive Oxygen Species; Autophagy; extracellular traps; Macrophages; | |
DOI : 10.3389/fcimb.2017.00053 | |
学科分类:生物科学(综合) | |
来源: Frontiers | |
【 摘 要 】
Aflatoxins are a group of highly toxic mycotoxins with high carcinogenicity that are commonly found in foods. Aflatoxin B1 (AFB1) is the most toxic member of the aflatoxin family. A recent study reported that AFB1 can induce autophagy, but whether AFB1 can induce extracellular traps (ETs) and the relationships among innate immune responses, reactive oxygen species (ROS), and autophagy and the ETs induced by AFB1 remain unknown. Here, we demonstrated that AFB1 induced a complete autophagic process in macrophages (MФ) (THP-1 cells and RAW264.7 cells). In addition, AFB1 induced the generation of MФ ETs (METs) in a dose-dependent manner. In particular, the formation of METs significantly reduced the AFB1 content. Further analysis using specific inhibitors showed that the inhibition of either autophagy or ROS prevented MET formation caused by AFB1, indicating that autophagy and ROS were required for AFB1-induced MET formation. The inhibition of ROS prevented autophagy, indicating that ROS generation occurred upstream of AFB1-induced autophagy. Taken together, these data suggest that AFB1 induces ROS-mediated autophagy and ETs formation and an M1 phenotype in MФ.
【 授权许可】
CC BY
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