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J Immunol. 2009 Sep 15;183(6):3578-81. doi: 10.4049/jimmunol.0901323. Epub 2009 Aug 14.

Cutting edge: Candida albicans hyphae formation triggers activation of the Nlrp3 inflammasome.

Author information

1
Division of Infectious Diseases, University of Iowa, Iowa City, IA 52242, USA.

Abstract

The proinflammatory cytokine IL-1beta plays an important role in antifungal immunity; however, the mechanisms by which fungal pathogens trigger IL-1beta secretion are unclear. In this study we show that infection with Candida albicans is sensed by the Nlrp3 inflammasome, resulting in the subsequent release of IL-1beta. The ability of C. albicans to switch from a unicellular yeast form into a filamentous form is essential for activation of the Nlrp3 inflammasome, as C. albicans mutants incapable of forming hyphae were defective in their ability to induce macrophage IL- 1beta secretion. Nlrp3-deficient mice also demonstrated increased susceptibility to infection with C. albicans, which is consistent with a key role for Nlrp3 in innate immune responses to the pathogen C. albicans.

PMID:
19684085
PMCID:
PMC2739101
DOI:
10.4049/jimmunol.0901323
[Indexed for MEDLINE]
Free PMC Article

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