期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 40, 期 3, 页码 764-769出版社
WILEY
DOI: 10.1002/eji.200939996
关键词
Brain endothelial cells; Cerebral Malaria; Inflammasome
类别
资金
- Swiss Science Foundation
- Swiss Society for Medical and Biological Stipends
- NIH [T32-HL007517, AI063331, AI064748]
- Arthritis Foundation
- JST
- MEXT
Cerebral malaria is the most severe complication of Plasmodium falciparum infection in humans and the pathogenesis is still unclear. Using the P. berghei ANKA infection model of mice, we investigated a potential involvement of Nlrp3 and the inflammasome in the pathogenesis of cerebral malaria. Nlrp3 mRNA expression was upregulated in brain endothelial cells after exposure to P. berghei ANKA. Although beta-hematin, a synthetic compound of the parasites heme polymer hemozoin, induced the release of IL-1 beta in macrophages through Nlrp3, we did not obtain evidence for a role of IL-1 beta in vivo. Nlrp3 knock-out mice displayed a delayed onset of cerebral malaria; however, mice deficient in caspase-1, the adaptor protein ASC or the IL-1 receptor succumbed as WT mice. These results indicate that the role of Nlrp3 in experimental cerebral malaria is independent of the inflammasome and the IL-1 receptor pathway.
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