期刊
SCIENTIFIC REPORTS
卷 9, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-019-44125-2
关键词
-
资金
- Sao Paulo Research Foundation (FAPESP, Brazil) [2013/07140-2, 2015/20432-8]
- National Council for Scientific and Technological Development (CNPq, Brazil) [303676/2014-0, 448765/2014-4]
- FAPESP [2013/09176-4, 2015/25874-9]
Malaria causes hepatic inflammation and damage, which contribute to disease severity. The pro-inflammatory cytokine interleukin (IL)-1 alpha is released by non-hematopoietic or hematopoietic cells during liver injury. This study established the role of IL-1 alpha in the liver pathology caused by blood-stage P. chabaudi malaria. During acute infection, hepatic inflammation and necrosis were accompanied by NLRP3 inflammasome-independent IL-1 alpha production. Systemically, IL-1 alpha deficiency attenuated weight loss and hypothermia but had minor effects on parasitemia control. In the liver, the absence of IL-1 alpha reduced the number ofTUNEL(+) cells and necrotic lesions. This finding was associated with a lower inflammatory response, including TNF-alpha. production. The main source of IL-1 alpha in the liver of infected mice was inflammatory cells, particularly neutrophils. The implication of IL-1 alpha in liver inflammation and necrosis caused by P. chabaudi infection, as well as in weight loss and hypothermia, opens up new perspectives for improving malaria outcomes by inhibiting IL-1 signaling.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据