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Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
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Experimental cerebral malaria progresses independently of the Nlrp3 inflammasome

Thornik Reimer1, Michael H Shaw, Luigi Franchi

  • 1Department of Pathology and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI 48109, USA.

European Journal of Immunology
|December 2, 2009
PubMed

Insights

Nlrp3 inflammasome activation is not essential for cerebral malaria pathogenesis. Nlrp3 plays a role independent of IL-1beta signaling in this severe Plasmodium falciparum complication.

Area of Science:

  • Immunology
  • Pathology
  • Infectious Diseases

Background:

  • Cerebral malaria, a severe Plasmodium falciparum complication, has unclear pathogenesis.
  • The role of Nlrp3 inflammasome in cerebral malaria requires further investigation.

Purpose of the Study:

  • To investigate the involvement of Nlrp3 and the inflammasome in experimental cerebral malaria pathogenesis.
  • To elucidate the specific pathways mediated by Nlrp3 in this condition.

Main Methods:

  • Utilized the P. berghei ANKA mouse model for experimental cerebral malaria.
  • Analyzed Nlrp3 mRNA expression in brain endothelial cells.
  • Investigated the effects of beta-hematin on IL-1beta release in macrophages.
  • Compared disease progression in Nlrp3 knockout mice versus wild-type and inflammasome-component deficient mice.

Main Results:

  • Nlrp3 mRNA expression was upregulated in brain endothelial cells during P. berghei ANKA infection.
  • Beta-hematin induced Nlrp3-dependent IL-1beta release in macrophages, but IL-1beta did not appear to play a role in vivo.
  • Nlrp3 knockout mice showed a delayed onset of cerebral malaria.
  • Mice deficient in caspase-1, ASC, or the IL-1 receptor exhibited outcomes similar to wild-type mice.

Conclusions:

  • Nlrp3 contributes to experimental cerebral malaria pathogenesis independently of the inflammasome and IL-1 receptor signaling.
  • The findings suggest a novel, inflammasome-independent role for Nlrp3 in cerebral malaria.

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