期刊
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
卷 22, 期 9, 页码 4056-4067出版社
WILEY
DOI: 10.1111/jcmm.13673
关键词
acute liver failure; interleukin-6; monocyte; non-human primate
资金
- National Key Clinical Project, National Natural Science Foundation of China [81570564]
- Major Science and Technology Project of Science & Technology Department of Sichuan Province [2017JY0029, 2014SZ0122, 2014SZ0027]
Acute liver failure (ALF) is associated with high mortality, and a poor understanding of the underlying pathophysiology has resulted in a lack of effective treatments so far. Here, using an amatoxin-induced rhesus monkey model of ALF, we panoramically revealed the cellular and molecular events that lead to the development of ALF. The challenged monkeys with toxins underwent a typical course of ALF including severe hepatic injury, systemic inflammation and eventual death. Adaptive immune was not noticeably disturbed throughout the progress of ALF. A systematic examination of serum factors and cytokines revealed that IL-6 increase was the most rapid and drastic. Interestingly, we found that IL-6 was mainly produced by circulating monocytes. Furthermore, ablation of monocyte-derived IL-6 in mice decreased liver injury and systemic inflammation following chemical injection. Our findings reveal a critical role of circulating monocytes in initiating and accelerating ALF, indicating a potential therapeutic target in clinical treatment for ALF.
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