| First Author | Reimer T | Year | 2010 |
| Journal | Eur J Immunol | Volume | 40 |
| Issue | 3 | Pages | 764-9 |
| PubMed ID | 19950187 | Mgi Jnum | J:157782 |
| Mgi Id | MGI:4436965 | Doi | 10.1002/eji.200939996 |
| Citation | Reimer T, et al. (2009) Experimental cerebral malaria progresses independently of the Nlrp3 inflammasome. Eur J Immunol 40(3):764-769 |
| abstractText | 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-1beta in macrophages through Nlrp3, we did not obtain evidence for a role of IL-1beta 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. |
